bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Strud crustacean fauna (Late Devonian, Belgium): updated review and palaeoecology of an early continental ecosystem
Authors: Gueriau Pierre , Rabet Nicolas , Du Tien Hat Eva 
Published: January 2018

ABSTRACTArthropods were the first known animals to colonise land habitats, with myriapods and arachnids having done so at least by the Silurian. Much later, several lineages of Pancrustacea (hexapods and the paraphyletic crustaceans) also ventured onto land; the hexapods by the Early Devonian, and later at least four other groups of crustaceans, namely isopods, amphipods, ostracods and decapods, most of which generally colonised the continental water bodies. All faced a series of challenges (in particular: gas exchange; desiccation; reproduction; osmoregulation; and exposure to ultraviolet radiation), resulting in many morphological, physiological and ecological adaptations. Nonetheless, whether they reached land via saltwater or freshwater remains poorly documented, mainly because relevant localities are few. The Famennian (Late Devonian) Strud locality in Belgium provided an exceptional source of information on early aquatic continental ecosystems and their plant, vertebrate and arthropod colonisers at a crucial step in the terrestrialisation process. Here, we review and update its crustacean fauna, which inhabited floodplain and temporary pool waters. New anatomical details of the notostracanStrudops goldenbergiLagebroet al., 2015, as well as a new genus and species of spinicaudatan, are described. We also discuss the ecology of this unique, early continental ecosystem and the insights it gives into the terrestrialisation process.
Amberground pholadid bivalve borings and inclusions in Burmese amber: implications for proximity of resin-producing forests to brackish waters, and the age of the amber
Authors: Smith Ru D. A. , Ross Andrew J. 
Published: January 2018

ABSTRACTClavate (club-shaped) structures rimming mid-Cretaceous Burmese amber from Myanmar, previously misdiagnosed as fungal sporocarps, are shown to be domichnia (crypts) of martesiine bivalves (Pholadidae: Martesiinae). They are similar in form toTeredolites clavatusLeymerie, 1842 andGastrochaenolites lapidicusKelly & Bromley, 1984; however, the former identification is preferable, given that they are martesiine crypts in amber as opposed to a lithic substrate. Cross-cutting relationships between the clavate features and inclusions in the amber demonstrate that the features post-date hardening of the resin. The fills of the crypts are variable, including sand grade sediment of very fine to coarse sand grainsize, and sparry calcite cements. In some cases, the articulated valves of the pholadid bivalve responsible are visible inside the borings. However, one remarkable specimen contains two pairs of articulated shells ‘floating’ in amber, not associated with crypts; an observation that suggests that the resin was still liquid or soft when the bivalves were trapped in the resin. One individual is associated with an irregular sediment-filled feature and shows shell breakage. Formation of a solid rim around a liquid central volume has been documented in subaqueous bodies of resin in modern swamp forests, and argues for a close proximity between the amber-producing trees and a brackish water habitat for the bivalves. The presence of pyrite as thin films and crystal groups within Burmese amber is further consistent with such a depositional environment. Comparison of the size of pholadid body fossils with growth rates of modern equivalents allows the duration of boring activities to be estimated and suggests that small fossil pholadids in Burmese amber became trapped and died within 1–2 weeks of having settled on the resin. Larger examples present within well-formed domichnia formed in hardened resin. Since ‘hardground’ describes early lithified sediment as a substrate and ‘woodground’ describes wood as a substrate, the term ‘amberground’ is used here to described borings in an amber substrate.
Lack of pronounced changes in the expression of fatty acid handling proteins in adipose tissue and plasma of morbidly obese humans
Authors: Grzegorczyk Ewa Anna , Harasim-Symbor Ewa , Lukaszuk Bartlomiej , Harasiuk Dorota , Choromanska Barbara , Mysliwiec Piotr , Zendzian-Piotrowska Malgorzata , Chabowski Adrian 
Published: January 2018

Abstract
Background/Objectives
Fatty acid handling proteins are involved in the process of accumulation of lipids in different fat tissue depots. Thus, the aim of the study was to estimate the expression of both fatty acid transport and binding proteins in the subcutaneous (SAT) and visceral adipose tissue (VAT) of patients with morbid obesity without metabolic syndrome, as well as the plasma concentrations of these transporters.

Subjects/Methods
Protein (Western blotting) and mRNA (Real-time PCR) expression of selected fatty acid handling proteins was assessed in the visceral and subcutaneous adipose tissue of 30 patients with morbid obesity. The control group consisted of 10 lean age-matched patients. Plasma levels of fatty acid protein transporters were also evaluated using ELISA method. Moreover, total plasma fatty acid composition and concentration was determined by gas-liquid chromatography (GLC).

Results
Significant increase in fatty acid translocase (FAT/CD36) mRNA (P = 0.03) and plasmalemmal (P = 0.01) expression was observed in VAT of patients with morbid obesity vs. lean subjects together with elevation of lipoprotein lipase (LPL), as well as peroxisome proliferator-activated receptor γ (PPARγ) in both examined compartments of adipose tissue. Moreover, in obese subjects plasma concentration of RBP4 was markedly elevated (P = 0.04) and sCD36 level presented a tendency for an increase (P = 0.08) with concomitant lack of changes in FABP4 concentration (P > 0.05).

Conclusions
Fatty acid transport into adipocytes may be, at least in part, related to the increased expression of FAT/CD36 in the VAT of morbidly obese patients, which is accompanied by augmented expression of LPL, as well as PPARγ. Probably, alternations in plasma concentrations of RBP4 and sCD36 in obese patients are associated with “unhealthy” fat distribution.
Exposure to famine in early life and chronic kidney diseases in adulthood
Authors: Wang Ningjian , Ning Zhiyuan , Xia Fangzhen , Chen Chi , Cheng Jing , Chen Yi , Lu Yingli 
Published: January 2018

Abstract
Objective
Chronic kidney disease (CKD) is an increasing contributor to the global disease burden. Previous findings indicated that exposure to famine in early life was associated with various metabolic diseases and urinary protein levels. We aimed to assess whether the exposure to China’s Great Famine 1959–1962 during fetal or childhood period was associated with glomerular filtration rate (GFR) and risk of CKD (eGFR<60 mL/min per 1.73 m2) in adulthood.

Materials and methods
SPECT-China was a population-based observational study in 2014–2015. Totally, 5124 women were included from SPECT-China study. Based on the birth year, they were divided into fetal-exposed (1959–1962), childhood-exposed (1949–1958), adolescence/young adult-exposed (1921–1948), and non-exposed (1963–1974, reference). The estimated glomerular filtration rate (eGFR) was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. CKD was defined as eGFR less than 60 mL/min per 1.73 m2.

Results
Compared with the non-exposed, fetal exposure to famine was significantly associated with lower eGFR (B −1.47, 95%CI −2.81, −1.13) and greater risk of having CKD (OR 2.85, 95%CI 1.25, 6.50) in the crude model adjusting age. Further adjustments for demographic variables, body mass index, diabetes, and blood pressure did not qualitatively change the association (eGFR B −1.35, 95%CI −2.67, −0.04; CKD OR 2.42, 95%CI 1.05, 5.58). This association was not found in childhood-exposed and adolescence/young adult-exposed individuals.

Conclusions
Prenatal exposure to famine may have long-term effects on declined GFR and the development of CKD in humans. thus, fetal stage may be an important time window to prevent CKD in later life.
The stage of soil development modulates rhizosphere effect along a High Arctic desert chronosequence
Authors: Mapelli Francesca , Marasco Ramona , Fusi Marco , Scaglia Barbara , Tsiamis George , Rolli Eleonora , Fodelianakis Stilianos , Bourtzis Kostas , Ventura Stefano , Tambone Fulvia , Adani Fabrizio , Borin Sara , Daffonchio Daniele 
Published: January 2018

Abstract
In mature soils, plant species and soil type determine the selection of root microbiota. Which of these two factors drives rhizosphere selection in barren substrates of developing desert soils has, however, not yet been established. Chronosequences of glacier forelands provide ideal natural environments to identify primary rhizosphere selection factors along the changing edaphic conditions of a developing soil. Here, we analyze changes in bacterial diversity in bulk soils and rhizospheres of a pioneer plant across a High Arctic glacier chronosequence. We show that the developmental stage of soil strongly modulates rhizosphere community assembly, even though plant-induced selection buffers the effect of changing edaphic factors. Bulk and rhizosphere soils host distinct bacterial communities that differentially vary along the chronosequence. Cation exchange capacity, exchangeable potassium, and metabolite concentration in the soil account for the rhizosphere bacterial diversity. Although the soil fraction (bulk soil and rhizosphere) explains up to 17.2% of the variation in bacterial microbiota, the soil developmental stage explains up to 47.7% of this variation. In addition, the operational taxonomic unit (OTU) co-occurrence network of the rhizosphere, whose complexity increases along the chronosequence, is loosely structured in barren compared with mature soils, corroborating our hypothesis that soil development tunes the rhizosphere effect.
The emergence of metabolic heterogeneity and diverse growth responses in isogenic bacterial cells
Authors: Şimşek Emrah , Kim Minsu 
Published: January 2018

Abstract
Microorganisms adapt to frequent environmental changes through population diversification. Previous studies demonstrated phenotypic diversity in a clonal population and its important effects on microbial ecology. However, the dynamic changes of phenotypic composition have rarely been characterized. Also, cellular variations and environmental factors responsible for phenotypic diversity remain poorly understood. Here, we studied phenotypic diversity driven by metabolic heterogeneity. We characterized metabolic activities and growth kinetics of starved Escherichia coli cells subject to nutrient upshift at single-cell resolution. We observed three subpopulations with distinct metabolic activities and growth phenotypes. One subpopulation was metabolically active and immediately grew upon nutrient upshift. One subpopulation was metabolically inactive and non-viable. The other subpopulation was metabolically partially active, and did not grow upon nutrient upshift. The ratio of these subpopulations changed dynamically during starvation. A long-term observation of cells with partial metabolic activities indicated that their metabolism was later spontaneously restored, leading to growth recovery. Further investigations showed that oxidative stress can induce the emergence of a subpopulation with partial metabolic activities. Our findings reveal the emergence of metabolic heterogeneity and associated dynamic changes in phenotypic composition. In addition, the results shed new light on microbial dormancy, which has important implications in microbial ecology and biomedicine.
Beta-defensin 1, aryl hydrocarbon receptor and plasma kynurenine in major depressive disorder: metabolomics-informed genomics
Authors: Liu Duan , Ray Balmiki , Neavin Drew R. , Zhang Jiabin , Athreya Arjun P. , Biernacka Joanna M. , Bobo William V. , Hall-Flavin Daniel K. , Skime Michelle K. , Zhu Hongjie , Jenkins Gregory D. , Batzler Anthony , Kalari Krishna R. , Boakye-Agyeman Felix , Matson Wayne R. , Bhasin Swati S. , Mushiroda Taisei , Nakamura Yusuke , Kubo Michiaki , Iyer Ravishankar K. , Wang Liewei , Frye Mark A. , Kaddurah-Daouk Rima , Weinshilboum Richard M. 
Published: January 2018

AbstractMajor depressive disorder (MDD) is a heterogeneous disease. Efforts to identify biomarkers for sub-classifying MDD and antidepressant therapy by genome-wide association studies (GWAS) alone have generally yielded disappointing results. We applied a metabolomics-informed genomic research strategy to study the contribution of genetic variation to MDD pathophysiology by assaying 31 metabolites, including compounds from the tryptophan, tyrosine, and purine pathways, in plasma samples from 290 MDD patients. Associations of metabolite concentrations with depressive symptoms were determined, followed by GWAS for selected metabolites and functional validation studies of the genes identified. Kynurenine (KYN), the baseline plasma metabolite that was most highly associated with depressive symptoms, was negatively correlated with severity of those symptoms. GWAS for baseline plasma KYN concentrations identified SNPs across the beta-defensin 1 (DEFB1) and aryl hydrocarbon receptor (AHR) genes that were cis-expression quantitative trait loci (eQTLs) forDEFB1andAHRmRNA expression, respectively. Furthermore, theDEFB1locus was associated with severity of MDD symptoms in a larger cohort of 803 MDD patients. Functional studies demonstrated that DEFB1 could neutralize lipopolysaccharide-stimulated expression of KYN-biosynthesizing enzymes in monocytic cells, resulting in altered KYN concentrations in the culture media. In addition, we demonstrated that AHR was involved in regulating the expression of enzymes in the KYN pathway and altered KYN biosynthesis in cell lines of hepatocyte and astrocyte origin. In conclusion, these studies identified SNPs that were cis-eQTLs forDEFB1andAHRand, which were associated with variation in plasma KYN concentrations that were related to severity of MDD symptoms.
Epigenetics and cerebral organoids: promising directions in autism spectrum disorders
Authors: Forsberg Sheena Louise , Ilieva Mirolyuba , Maria Michel Tanja 
Published: January 2018

AbstractAutism spectrum disorders (ASD) affect 1 in 68 children in the US according to the Centers for Disease Control and Prevention (CDC). It is characterized by impairments in social interactions and communication, restrictive and repetitive patterns of behaviors, and interests. Owing to disease complexity, only a limited number of treatment options are available mainly for children that alleviate but do not cure the debilitating symptoms. Studies confirm a genetic link, but environmental factors, such as medications, toxins, and maternal infection during pregnancy, as well as birth complications also play a role. Some studies indicate a set of candidate genes with different DNA methylation profiles in ASD compared to healthy individuals. Thus epigenetic alterations could help bridging the gene–environment gap in deciphering the underlying neurobiology of autism. However, epigenome-wide association studies (EWAS) have mainly included a very limited number of postmortem brain samples. Hence, cellular models mimicking brain development in vitro will be of great importance to study the critical epigenetic alterations and when they might happen. This review will give an overview of the state of the art concerning knowledge on epigenetic changes in autism and how new, cutting edge expertise based on three-dimensional (3D) stem cell technology models (brain organoids) can contribute in elucidating the multiple aspects of disease mechanisms.
DNA methylome variation in a perinatal nurse-visitation program that reduces child maltreatment: a 27-year follow-up
Authors: O’Donnell Kieran J. , Chen Li , MacIsaac Julia L. , McEwen Lisa M. , Nguyen Thao , Beckmann Katherine , Zhu Yuecai , Chen Lawrence Ming , Brooks-Gunn Jeanne , Goldman David , Grigorenko Elena L. , Leckman James F. , Diorio Josie , Karnani Neerja , Olds David L. , Holbrook Joanna D. , Kobor Michael S. , Meaney Michael J. 
Published: January 2018

AbstractThis study reveals the influence of child maltreatment on DNA methylation across the genome and provides the first evidence that a psychosocial intervention program, the Nurse Family Partnership (NFP), which targets mothers at risk for abusive parenting, associates with variation in the DNA methylome in adult offspring. The 188 participants were born to women randomly assigned to control (n = 99) or nurse-visited intervention groups (n = 89) and provided blood samples and a diagnostic interview at age 27 years. Interindividual variation in the blood DNA methylome was described using principal components (PC) scores derived from principal component analysis and showed that the NFP program (PC10: p = 0.029) and a history of abuse/neglect (PC1: p = 0.029, PC2: p = 0.009) significantly associated with DNA methylome variation at 27 years of age independent of gender, ancestry, cellular heterogeneity, and a polygenic risk index for major psychiatric disorders. The magnitude of the association between child maltreatment and DNA methylation was reduced when accounting for lifestyle factors, including smoking. These findings reflect the sustained impact of both childhood adversity as well as intervention programs that target such adversity on the epigenome but highlight the need for prospective longitudinal studies of DNA methylome variation in the context of early intervention programs.
Metabotropic glutamate receptor 5 binding in male patients with alcohol use disorder
Authors: Akkus Funda , Mihov Yoan , Treyer Valerie , Ametamey Simon M. , Johayem Anass , Senn Smeralda , Rösner Susanne , Buck Alfred , Hasler Gregor 
Published: January 2018

AbstractGlutamate signaling plays a major role in addiction. Preclinical research strongly suggests an implication of G-protein-coupled metabotropic glutamate receptor subtype 5 (mGluR5) in nicotine addiction and alcohol use disorder. In humans, smoking is related to a global reduction in mGluR5 availability. In the present study, we investigated mGluR5 in vivo in patients with alcohol use disorder without the confounding effects of smoking. A total of 14 male subjects with alcohol use disorder and at least a 25-day abstinence and 14 matched male non-smoking healthy controls were included in the study. We employed positron emission tomography (PET) with the mGluR5-specific radiotracer [11C]ABP688, using a bolus/infusion protocol. We found increased mGluR5 DVR in several regions within the temporal lobe in patients, as compared to controls. The largest between-group difference was in the amygdala. There was a marked positive relation between mGluR5 DVR in the anterior cingulate and mGluR5 DVR in the orbitofrontal cortex in patients, but not in controls. In patients, lower temptation to drink was related to higher amygdala mGluR5 DVR. We did not find altered mGluR5 DVR in the basal ganglia of subjects recovering from alcohol use disorder. In conclusion, our study provides clinical evidence for altered mGluR5 signaling in the amygdala in alcohol use disorder. This alteration was associated with the temptation to drink. In addition, this study suggests abnormal mGluR5 signaling in a network underlying reward-related behavioral flexibility. These findings strengthen the case for pharmacological agents acting on mGluR5 as promising candidates for the treatment of alcohol use disorder.
Preliminary evidence for genetic overlap between body mass index and striatal reward response
Authors: Lancaster T. M. , Ihssen I. , Brindley L. M. , Linden D. E. 
Published: January 2018

AbstractThe reward-processing network is implicated in the aetiology of obesity. Several lines of evidence suggest obesity-linked genetic risk loci (such as DRD2 and FTO) may influence individual variation in body mass index (BMI) through neuropsychological processes reflected in alterations in activation of the striatum during reward processing. However, no study has tested the broader hypotheses that (a) the relationship between BMI and reward-related brain activation (measured through the blood oxygenation-dependent (BOLD) signal) may be observed in a large population study and (b) the overall genetic architecture of these phenotypes overlap, an assumption critical for the progression of imaging genetic studies in obesity research. Using data from the Human Connectome Project (N = 1055 healthy, young individuals: average BMI = 26.4), we first establish a phenotypic relationship between BMI and ventral striatal (VS) BOLD during the processing of rewarding (monetary) stimuli (β = 0.44, P = 0.013), accounting for potential confounds. BMI and VS BOLD were both significantly influenced by additive genetic factors (H2r = 0.57; 0.12, respectively). Further decomposition of this variance suggested that the relationship was driven by shared genetic (ρg = 0.47, P = 0.011), but not environmental (ρE = −0.07, P = 0.29) factors. To validate the assumption of genetic pleiotropy between BMI and VS BOLD, we further show that polygenic risk for higher BMI is also associated with increased VS BOLD response to appetitive stimuli (calorically high food images), in an independent sample (N = 81; PFWE−ROI < 0.005). Together, these observations suggest that the genetic factors link risk to obesity to alterations within key nodes of the brain's reward circuity. These observations provide a basis for future work exploring the mechanistic role of genetic loci that confer risk for obesity using the imaging genetics approach.
Glucose-6-phosphate dehydrogenase is indispensable in embryonic development by modulation of epithelial-mesenchymal transition via the NOX/Smad3/miR-200b axis
Authors: Wu Yi-Hsuan , Lee Ying-Hsuan , Shih Hung-Yu , Chen Shih-Hsiang , Cheng Yi-Chuan , Tsun-Yee Chiu Daniel 
Published: January 2018

AbstractGlucose-6-phosphate dehydrogenase (G6PD) is a housekeeping enzyme involved in the pentose phosphate shunt for producing nicotinamide adenine dinucleotide phosphate (NADPH). Severe G6PD deficiency leads to embryonic lethality, but the underlying mechanism is unclear. In the current study, the effects of G6PD on epithelial–mesenchymal transition (EMT), especially during embryonic development, were investigated. The knockdown of G6PD induced morphological changes, accompanied by the suppression of epithelial markers, E-cadherin and β-catenin, in A549 and MDCK cells. Such modulation of EMT was corroborated by the enhancement of migration ability in G6PD-knockdown A549 cells. Zebrafish embryos with g6pd knockdown exhibited downregulation of the E-cadherin/β-catenin adhesion molecules and impaired embryonic development through reduction in epiboly rate and increase in cell shedding at the embryo surface. The dysregulation in zebrafish embryonic development caused by g6pd knockdown could be rescued through human G6PD or CDH1 (E-cadherin gene) cRNA coinjection. The Smad3/miR-200b axis was dysregulated upon G6PD knockdown, and the reconstitution of SMAD3 in G6PD-knockdown A549 cells restored the expression of E-cadherin/β-catenin. The inhibition of NADPH oxidase (NOX) activation through the loss of p22phox signaling was involved in the dysregulation of the Smad3/miR-200b axis upon G6PD knockdown. The reconstitution of G6PD led to the recovery of the regulation of NOX/Smad3/miR-200b signaling and increased the expression of E-cadherin/β-catenin in G6PD-knockdown cells. Thus, these results suggest that in the EMT process, G6PD plays an important regulatory role as an integral component of the NOX/Smad3/miR-200b axis.