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[PMID]: 29524876
[Au] Autor:Chang Z; Tian L; Wu M; Dong X; Peng J; Pan B
[Ad] Address:Faculty of Environmental Science & Engineering, Kunming University of Science & Technology, Kunming 650500, PR China.
[Ti] Title:Molecular markers of benzene polycarboxylic acids in describing biochar physiochemical properties and sorption characteristics.
[So] Source:Environ Pollut;237:541-548, 2018 Mar 07.
[Is] ISSN:1873-6424
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Biochar function in soil is based on properties such as sorption characteristics, and these are expected to change throughout the life cycle of the biochar. Because biochar particles cannot easily be separated from soil particles, this change is seldom investigated. Biochar-related molecular markers, such as benzene polycarboxylic acids (BPCAs) are promising tools for studying the properties of biochars in complex environmental matrices. In this study, biochars were derived from corn straw and pine wood sawdust at 200-500 °C, and their aging was simulated with NaClO. Biochar properties were characterized by elemental analysis, BET surface characterization and BPCA molecular marker analysis. Chemical oxidation decreased the surface area (SA) but increased the O content of biochars. The oxidation decreased the amount of biochars, with a mass loss in the range of 10-55%. A similar mass loss was also observed for BPCAs and was negatively related to both the pyrolysis temperature and the extent of the condensed structure (higher aromaticity). The biochar amounts were calculated quantitatively using the sum of BPCA contents, with a conversion factor (the ratio of biochar amount to BPCA content) in the range of 3.3-5.5, and were negatively related to the B5CA content. Three model pollutants, namely, bisphenol A (BPA), sulfamethoxazole (SMX), and phenanthrene (PHE), were chosen to study the sorption characteristics of biochar before and after oxidation. Chemical oxidation generally increased SMX sorption but decreased PHE sorption. The nonlinear factor n, based on Freundlich equation modeling, was negatively related to B6CA for all three chemicals. The BPCA molecular markers, especially B5CA and B6CA, were correlated to the biochar properties before and after oxidation and are thus a potentially useful technique for describing the characteristics of biochar in the environment.
[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]: 29524756
[Au] Autor:Swanberg KM; Prinsen H; Coman D; de Graaf RA; Juchem C
[Ad] Address:Department of Biomedical Engineering, Columbia University Fu Foundation School of Engineering and Applied Science, 1210 Amsterdam Ave., New York, NY 10027, United States; Department of Radiology and Biomedical Imaging, Yale University School of Medicine, 330 Cedar Street, New Haven, CT 06520, United
[Ti] Title:Quantification of glutathione transverse relaxation time T using echo time extension with variable refocusing selectivity and symmetry in the human brain at 7 Tesla.
[So] Source:J Magn Reson;290:1-11, 2018 Mar 01.
[Is] ISSN:1096-0856
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Glutathione (GSH) is an endogenous antioxidant implicated in numerous biological processes, including those associated with multiple sclerosis, aging, and cancer. Spectral editing techniques have greatly facilitated the acquisition of glutathione signal in living humans via proton magnetic resonance spectroscopy, but signal quantification at 7 Tesla is still hampered by uncertainty about the glutathione transverse decay rate T relative to those of commonly employed quantitative references like N-acetyl aspartate (NAA), total creatine, or water. While the T of uncoupled singlets can be derived in a straightforward manner from exponential signal decay as a function of echo time, similar estimation of signal decay in GSH is complicated by a spin system that involves both weak and strong J-couplings as well as resonances that overlap those of several other metabolites and macromolecules. Here, we extend a previously published method for quantifying the T of GABA, a weakly coupled system, to quantify T of the strongly coupled spin system glutathione in the human brain at 7 Tesla. Using full density matrix simulation of glutathione signal behavior, we selected an array of eight optimized echo times between 72 and 322 ms for glutathione signal acquisition by J-difference editing (JDE). We varied the selectivity and symmetry parameters of the inversion pulses used for echo time extension to further optimize the intensity, simplicity, and distinctiveness of glutathione signals at chosen echo times. Pairs of selective adiabatic inversion pulses replaced nonselective pulses at three extended echo times, and symmetry of the time intervals between the two extension pulses was adjusted at one extended echo time to compensate for J-modulation, thereby resulting in appreciable signal-to-noise ratio and quantifiable signal shapes at all measured points. Glutathione signal across all echo times fit smooth monoexponential curves over ten scans of occipital cortex voxels in nine subjects. The T of glutathione was calculated to be 145.0 ±â€¯20.1 ms (mean ±â€¯standard deviation); this result was robust within one standard deviation to changes in metabolite fitting baseline corrections and removal of individual data points on the signal decay curve. The measured T of NAA (222.1 ±â€¯24.7 ms) and total creatine (153.0 ±â€¯19.9 ms) were both higher than that calculated for GSH. Apparent glutathione concentration quantified relative to both reference metabolites increased by up to 32% and 6%, respectively, upon correction with calculated T values, emphasizing the importance of considering T relaxation differences in the spectroscopic measurement of these metabolites, especially at longer echo times.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 376744 MEDLINE  
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[PMID]: 29524680
[Au] Autor:van den Brink AMA; Gerritsen DL; de Valk MMH; Mulder AT; Oude Voshaar RC; Koopmans RTCM
[Ad] Address:De Waalboog, 'Joachim en Anna', Center for Specialized Geriatric Care, Postbus 31071, 6503 CB, Nijmegen, The Netherlands; Radboud University Medical Center, Radboud Institute for Health Sciences, Department of Primary and Community Care, Postbus 9101, 6500 HB, Nijmegen, The Netherlands. Electronic a
[Ti] Title:What do nursing home residents with mental-physical multimorbidity need and who actually knows this? A cross-sectional cohort study.
[So] Source:Int J Nurs Stud;81:89-97, 2018 Feb 26.
[Is] ISSN:1873-491X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Aging societies will bring an increase in the number of long-term care residents with mental-physical multimorbidity. To optimize care for these residents, it is important to study their care needs, since unmet needs lower quality of life. To date, knowledge about care needs of residents with mental-physical multimorbidity is limited. The aim of this study was to explore (un)met care needs of residents with mental-physical multimorbidity and determinants of unmet needs. METHODS: Cross-sectional cohort study among 141 residents with mental-physical multimorbidity without dementia living in 17 geronto-psychiatric nursing home units across the Netherlands. Data collection consisted of chart review, semi-structured interviews, (brief) neuropsychological testing, and self-report questionnaires. The Camberwell Assessment of Need for the Elderly (CANE) was used to rate (un)met care needs from residents' and nursing staff's perceptions. Descriptive and multivariate regression analyses were conducted. RESULTS: Residents reported a mean number of 11.89 needs (SD 2.88) of which 24.2% (n = 2.88, SD 2.48) were unmet. Nursing staff indicated a mean number of 14.73 needs (SD 2.32) of which 10.8% (n = 1.59, SD 1.61) were unmet. According to the residents, most unmet needs were found in the social domain as opposed to the psychological domain as reported by the nursing staff. Different opinions between resident and nursing staff about unmet needs was most common in the areas accommodation, company, and daytime activities. Further, nearly half of the residents indicated 'no need' regarding behavior while the nursing staff supposed that the resident did require some kind of support. Depression, anxiety and less care dependency were the most important determinants of unmet needs. CONCLUSIONS: Systematic assessment of care needs showed differences between the perspectives of resident and nursing staff. These should be the starting point of a dialogue between them about needs, wishes and expectations regarding care. This dialogue can subsequently lead to the most optimal individually tailored care plan. To achieve this, nurses with effective communication and negotiation skills, are indispensable.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 376744 MEDLINE  
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[PMID]: 29524633
[Au] Autor:He C; Zhou C; Kennedy BK
[Ad] Address:Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA 94945, USA.
[Ti] Title:The yeast replicative aging model.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:It has been nearly three decades since the budding yeast Saccharomyces cerevisiae became a significant model organism for aging research and it has emerged as both simple and powerful. The replicative aging assay, which interrogates the number of times a "mother" cell can divide and produce "daughters," has been a stalwart in these studies, and genetic approaches have led to the identification of hundreds of genes impacting lifespan. More recently, cell biological and biochemical approaches have been developed to determine how cellular processes become altered with age. Together, the tools are in place to develop a holistic view of aging in this single-celled organism. Here, we summarize the current state of understanding of yeast replicative aging with a focus on the recent studies that shed new light on how aging pathways interact to modulate lifespan in yeast.
[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]: 29524490
[Au] Autor:Li Y; Guan S; Liu C; Chen X; Zhu Y; Xie Y; Wang J; Ji X; Li L; Li Z; Zhang Y; Zeng X; Li M
[Ad] Address:Department of Traditional Chinese Medicine, Shanghai Pudong Hopstital, Fudan University Pudong Medical Center, Shanghai 201399, China; Chuangchun University of Chinese Medicine, Changchun, Jilin 130117, China.
[Ti] Title:Neuroprotective effects of Coptis chinensis Franch polysaccharide on amyloid-beta (Aß)-induced toxicity in a transgenic Caenorhabditis elegans model of Alzheimer's disease (AD).
[So] Source:Int J Biol Macromol;, 2018 Mar 07.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:This study aims to investigate the neuroprotective effects of Coptis chinensis Franch polysaccharide (CCP) on Aß transgenic CL4176 Caenorhabditis elegans, as well as its mechanism of action. The results in life span experiment showed that CCP could significantly increase the lifespan of C. elegans and the effect is in the descending order of 100 mg/L > 500 mg/L > 200 mg/L. The behavioral experiments also demonstrated that CCP at the concentration of 100 mg/L could delay the paralysis rate of C. elegans, which was significantly different from the control group. In terms of Aß toxicity in C. elegans, morphological observation using Thioflavin S staining method indicated that the deposition of Aß protein in the head area of the untreated C. elegans was much more than those in the CCP (100 mg/L)-treated CL4176. In line with this finding, fluorogenic quantitative real-time PCR confirmed that the transcriptional levels of HSP16.2 (Y46H3A.D) and HSP16.41 (Y46H3A.E) in C. elegans was 21 times and 79 times higher than those in untreated control. Thus, these data demonstrate that CCP could reduce Aß-induced toxicity by delaying the aging, decreasing the rate of paralysis, inhibiting the deposition of Aß, and increasing the expression levels of HSP genes in transgenic C. elegans.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 376744 MEDLINE  
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[PMID]: 29524468
[Au] Autor:Belblidia H; Leger M; Abdelmalek A; Quiedeville A; Calocer F; Boulouard M; Jozet-Alves C; Freret T; Schumann-Bard P
[Ad] Address:Université de Caen Normandie, UFR SANTE, Faculté des Sciences Pharmaceutiques, INSERM UMR 1075, COMETE-MOBILITES "Vieillissement, Pathologie, Santé", 14032 Caen, France; Université des Sciences et de la Technologie Houari Boumediene USTHB, Département de biologie, Laboratoire de Neurosciences Compor
[Ti] Title:Characterizing age-related decline of recognition memory and brain activation profile in mice.
[So] Source:Exp Gerontol;, 2018 Mar 07.
[Is] ISSN:1873-6815
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Episodic memory decline is one of the earlier deficits occurring during normal aging in humans. The question of spatial versus non-spatial sensitivity to age-related memory decline is of importance for a full understanding of these changes. Here, we characterized the effect of normal aging on both non-spatial (object) and spatial (object location) memory performances as well as on associated neuronal activation in mice. Novel-object (NOR) and object-location (OLR) recognition tests, respectively assessing the identity and spatial features of object memory, were examined at different ages. We show that memory performances in both tests were altered by aging as early as 15 months of age: NOR memory was partially impaired whereas OLR memory was found to be fully disrupted at 15 months of age. Brain activation profiles were assessed for both tests using immunohistochemical detection of c-Fos (neuronal activation marker) in 3and 15 month-old mice. Normal performances in NOR task by 3 month-old mice were associated to an activation of the hippocampus and a trend towards an activation in the perirhinal cortex, in a way that did significantly differ with 15 month-old mice. During OLR task, brain activation took place in the hippocampus in 3 month-old but not significantly in 15 month-old mice, which were fully impaired at this task. These differential alterations of the object- and object-location recognition memory may be linked to differential alteration of the neuronal networks supporting these tasks.
[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]: 29524430
[Au] Autor:Abidi M; Khan MS; Ahmad S; Kausar T; Nayeem SM; Islam S; Ali A; Alam K; Moinuddin
[Ad] Address:Department of Biochemistry, Jawaharlal Nehru Medical College, AMU, Aligarh, India.
[Ti] Title:Biophysical and biochemical studies on glycoxidatively modified human low density lipoprotein.
[So] Source:Arch Biochem Biophys;, 2018 Mar 07.
[Is] ISSN:1096-0384
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Methylglyoxal (MGO), a reactive dicarbonyl metabolite is a potent arginine directed glycating agent which has implications for diabetes-related complications. Dicarbonyl metabolites are produced endogenously and in a state of misbalance, they contribute to cell and tissue dysfunction through protein and DNA modifications causing dicarbonyl stress. MGO is detoxified by glyoxalase 1 (GLO1) system in the cytoplasm. Reactive oxygen species (ROS) are known to aggravate the glycation process. Both the processes are closely linked, and their combined activity is often referred to as "glycoxidation" process. Glycoxidation of proteins has several consequences such as type 2 diabetes mellitus (T2DM), aging etc. In this study, we have investigated the glycation of low-density lipoprotein (LDL) using different concentrations of MGO for varied incubation time periods. The structural perturbations induced in LDL were analyzed by UV-Vis, fluorescence, circular dichroism spectroscopy, molecular docking studies, polyacrylamide gel electrophoresis, FTIR, thermal denaturation studies, Thioflavin T assay and isothermal titration calorimetry. The ketoamine moieties, carbonyl content and HMF content were quantitated in native and glycated LDL. Simulation studies were also done to see the effect of MGO on the secondary structure of the protein. We report structural perturbations, increased carbonyl content, ketoamine moieties and HMF content in glycated LDL as compared to native analog (native LDL). We report the structural perturbations in LDL upon modification with MGO which could obstruct its normal physiological functions and hence contribute to disease pathogenesis and associated complications.
[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]: 29524414
[Au] Autor:Liu P; Feng T; Zuo X; Wang X; Luo J; Li N; Han X; Zhu N; Xu S; Xu Y; Jin ZG; Si S
[Ad] Address:Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
[Ti] Title:A novel SIRT1 activator E6155 improves insulin sensitivity in type 2 diabetic KKA mice.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sirtuin 1 (SIRT1) is an NAD -dependent protein deacetylase that plays a critical role in controlling energy metabolism, stress response and aging. Hence, enhancing SIRT1 activity could be a potential therapeutic strategy to treat metabolic diseases such as diabetes. However, pharmacological activators for SIRT1 are scarce to date. In this study, using the optimized high throughput screening, we identified E6155, a piperazine 1, 4- diamide compound, as a new small molecular activator of SIRT1. We further found that E6155 significantly upregulated glucose uptake in cultured mouse liver cells and skeletal muscle cells through increasing SIRT1 deacetylase activity. In type 2 diabetic KKA mice, E6155 treatment markedly decreased the level of fasting glucose. Moreover, E6155 improved oral glucose tolerance and insulin tolerance. Euglycemic clamp and the homeostasis model assessment of insulin resistance index showed that E6155 ameliorated the insulin resistance and increased insulin sensitivity in diabetic mice. Mechanistically, we observed that the antidiabetic effects of E6155 were involved in SIRT1 dependent activation of LKB1/AMPK and IRS1/AKT pathways. In conclusion, our findings identified E6155 as a novel SIRT1 activator and suggested that E6155 could be a promising drug candidate for treating insulin resistance and diabetes.
[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]: 29520134
[Au] Autor:Du W; Liu J; Zhou J; Ye D; OuYang Y; Deng Q
[Ad] Address:Respiratory Diseases Group, the 6th Unit, Department of Internal Medicine, Guangzhou General Hospital of Guangzhou Military Command, Guangzhou 510010, China.
[Ti] Title:Obstructive sleep apnea, COPD, the overlap syndrome, and mortality: results from the 2005-2008 National Health and Nutrition Examination Survey.
[So] Source:Int J Chron Obstruct Pulmon Dis;13:665-674, 2018.
[Is] ISSN:1178-2005
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Objective: The aim of this study was to investigate the role of obstructive sleep apnea (OSA) on all-cause mortality in patients with COPD. Methods: Data for this cross-sectional study were obtained from the National Health and Nutrition Examination Survey (NHANES) data (year 2005-2008). Eligible subjects were ≥20 years who had no COPD or OSA (n=9,237), had only OSA (n=366), had only COPD (n=695), and had OSA/COPD overlap syndrome (n=90). Univariate and multivariate analyses were used to evaluate factors associated with overall mortality. Results: Multivariate analysis found that the COPD and OSA/COPD overlap syndrome groups had significantly higher chance of all-cause mortality than the group of subjects who did not have OSA or COPD (adjusted hazard ratio [HR] =1.5 for the COPD group and 2.4 for the overlap syndrome group) ( ≤0.007). Although not significant, having OSA/COPD overlap syndrome was associated with higher likelihood of death than COPD alone (HR =1.5; =0.160). Other factors associated with higher overall mortality were aging, poorer family status, current smoker, serum vitamin D deficiency, cardiovascular disease, history of cancer, diabetes, and impaired renal function. Conclusion: The present study found that COPD and OSA/COPD overlap syndrome were associated with higher all-cause mortality compared with patients without either disease and that OSA did not significantly increase mortality in patients with COPD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.2147/COPD.S148735

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[PMID]: 29520133
[Au] Autor:Xing W; Lv X; Gao W; Wang J; Yang Z; Wang S; Zhang J; Yan J
[Ad] Address:Zhejiang Provincial Key Laboratory of Geriatrics, Department of Geriatrics, Zhejiang Hospital.
[Ti] Title:Bone mineral density in patients with chronic heart failure: a meta-analysis.
[So] Source:Clin Interv Aging;13:343-353, 2018.
[Is] ISSN:1178-1998
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Objective: This study aimed to verify the existing relationship between bone mineral density (BMD) and chronic heart failure (CHF) by meta-analysis. Methods: Databases, including PubMed, Web of Science, and Chinese National Knowledge Infrastructure, published in English or Chinese up to February 28, 2017, were searched for studies on the association between CHF and BMD. Two independent reviewers collected the relevant articles. The standard mean deviation (SMD) and 95% confidence interval were calculated for BMD with fixed- and random-effect models. Subgroup and sensitivity analyses were also conducted. Results: A total of six studies (552 CHF and 243 non-CHF patients) were included. The results indicated that the patients with CHF had a lower total BMD compared with the non-CHF patients. Similar effects were also observed for femoral neck, arm, leg, and trunk BMD. However, no difference was observed in the lumbar spine BMD. The SMD of total BMD in New York Heart Association classes I or II (NYHA I or II) patients was -0.62, while that in NYHA III or IV patients was -0.87, and the SMD of femoral bone mineral density in NYHA I or II patients was -0.47, while that in NYHA III or IV patients was -1.07. Moreover, vitamin D and parathyroid hormone (PTH) were also found to be associated with CHF. Conclusion: Patients with CHF had a lower total BMD and femoral neck, arm, leg, or trochanter BMD than patients with non-CHF. Vitamin D reduced, whereas PTH increased, with the severity of CHF. The clinical significance of the present findings remains uncertain and should be confirmed by future studies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.2147/CIA.S154356


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