bluuebunny/crossref_metadata_2025_split huggingface dataset:
Maraviroc Reduces Arterial Stiffness in PI-Treated HIV-infected Patients
Authors: Piconi Stefania , Pocaterra Daria , Rainone Veronica , Cossu Maria , Masetti Michela , Rizzardini Giuliano , Clerici Mario , Trabattoni Daria 
Published: June 2016

AbstractThe Δ32-CCR5 deletion of the CCR5 receptor is protective toward coronary artery pathology and myocardial infarction. Maraviroc (MVC), a CCR5 antagonist, was recently introduced in the therapy of HIV infection; we evaluated whether this drug could modulate the atherosclerotic burden in aviremic PI-treated HIV-positive individuals who underwent MVC intensification. Thus, the effect of MVC on intima media thickness, arterial stiffness, metabolic parameters, pro-inflammatory cytokines, endothelial dysfunction, and microbial traslocation markers was analyzed in 6 aviremic PI-treated HIV-positive individuals and were compared to those obtained in 9 additional aviremic PI-treated subjects that were enrolled retrospectively from our outpatients cohort. MVC intensification resulted in a significant reduction in intima media thickness, pulse wave velocity and triglycerides compared to baseline. Notably, MVC was also associated with a significant reduction of IL-6, microbial translocation indexes, sICAM and sVCAM; these changes were maintained throughout the 6 months of MVC intensification. No significant modifications were observed in CD4 counts, HIV viral load, and cholesterolemia. Results herein support a role of CCR5 antagonists in reducing the cardiovascular risk in HIV-infection. The hampering of inflammation, microbial translocation and the improvement of endothelial function could justify the protective role of CCR5 antagonists on atherosclerotic burden.
Soil Potassium Deficiency Reduces Cotton Fiber Strength by Accelerating and Shortening Fiber Development
Authors: Yang Jia-Shuo , Hu Wei , Zhao Wenqing , Meng Yali , Chen Binglin , Wang Youhua , Zhou Zhiguo 
Published: June 2016

AbstractLow potassium (K)-induced premature senescence in cotton has been observed worldwide, but how it affects cotton fiber properties remain unclear. We hypothesized that K deficiency affects cotton fiber properties by causing disordered fiber development, which may in turn be caused by the induction of a carbohydrate acquisition difficulty. To investigate this issue, we employed a low-K-sensitive cotton cultivar Siza 3 and a low-K-tolerant cultivar Simian 3 and planted them in three regions of different K supply. Data concerning lint yield, Pn and main fiber properties were collected from three years of testing. Soil K deficiency significantly accelerated fiber cellulose accumulation and dehydration processes, which, together with previous findings, suggests that the low-K induced carbohydrate acquisition difficulty could cause disordered fiber development by stimulating the expression of functional proteins such as CDKA (cyclin-dependent kinase). As a result, fiber strength and lint weight were reduced by up to 7.8% and 2.1%, respectively. Additional quantitative analysis revealed that the degree of accelerated fiber development negatively correlated with fiber strength. According to the results of this study, it is feasible to address the effects of soil K deficiency on fiber properties using existing cultivation strategies to prevent premature senescence of cotton plants.
Ethoxyquin provides neuroprotection against cisplatin-induced neurotoxicity
Authors: Zhu Jing , Carozzi Valentina Alda , Reed Nicole , Mi Ruifa , Marmiroli Paola , Cavaletti Guido , Hoke Ahmet 
Published: June 2016

AbstractEthoxyquin was recently identified as a neuroprotective compound against toxic neuropathies and efficacy was demonstrated against paclitaxel-induced neurotoxicity in vivo. In this study we examined the efficacy of ethoxyquin in preventing neurotoxicity of cisplatin in rodent models of chemotherapy-induced peripheral neuropathy and explored its mechanism of action. Ethoxyquin prevented neurotoxicity of cisplatin in vitro in a sensory neuronal cell line and primary rat dorsal root ganglion neurons. In vivo, chronic co-administration of ethoxyquin partially abrogated cisplatin-induced behavioral, electrophysiological and morphological abnormalities. Furthermore, ethoxyquin did not interfere with cisplatin’s ability to induce tumor cell death in ovarian cancer cell line in vitro and in vivo. Finally, ethoxyquin reduced the levels of two client proteins (SF3B2 and ataxin-2) of a chaperone protein, heat shock protein 90 (Hsp90) when co-administered with cisplatin in vitro. These results implied that the neuroprotective effect of ethoxyquin is mediated through these two client proteins of Hsp90. In fact, reducing levels of SF3B2 in tissue-cultured neurons was effective against neurotoxicity of cisplatin. These findings suggest that ethoxyquin or other compounds that inhibit chaperone activity of Hsp90 and reduce levels of its client protein, SF3B2 may be developed as an adjuvant therapy to prevent neurotoxicity in cisplatin-based chemotherapy protocols.
The impact of individual and combined abiotic factors on daily otolith growth in a coral reef fish
Authors: Wenger Amelia S. , Whinney James , Taylor Brett , Kroon Frederieke 
Published: June 2016

AbstractCoral reefs are increasingly subjected to both local and global stressors, however, there is limited information on how reef organisms respond to their combined effects under natural conditions. This field study examined the growth response of the damselfish Neopomacentrus bankieri to the individual and combined effects of multiple abiotic factors. Turbidity, temperature, tidal movement, and wave action were recorded every 10 minutes for four months, after which the daily otolith growth of N. bankieri was aligned with corresponding abiotic conditions. Temperature was the only significant driver of daily otolith increment width, with increasing temperatures resulting in decreasing width. Although tidal movement was not a significant driver of increment width by itself, the combined effect of tidal movement and temperature had a greater negative effect on growth than temperature alone. Our results indicate that temperature can drive changes in growth even at very fine scales, and demonstrate that the cumulative impact of abiotic factors can be substantially greater than individual effects. As abiotic factors continue to change in intensity and duration, the combined impacts of them will become increasingly important drivers of physiological and ecological change.
Osteopontin deficiency reduces kidney damage from hypercholesterolemia in Apolipoprotein E-deficient mice
Authors: Pei Zouwei , Okura Takafumi , Nagao Tomoaki , Enomoto Daijiro , Kukida Masayoshi , Tanino Akiko , Miyoshi Ken-ichi , Kurata Mie , Higaki Jitsuo 
Published: June 2016

AbstractHypercholesterolemia is a well-established risk factor for kidney injury, which can lead to chronic kidney disease (CKD). Osteopontin (OPN) has been implicated in the pathology of several renal conditions. This study was to evaluate the effects of OPN on hypercholesterolemia induced renal dysfunction. Eight-week-old male mice were divided into 4 groups: apolipoprotein E knockout (ApoE−/−) and ApoE/OPN knockout (ApoE−/−/OPN−/−) mice fed a normal diet (ND) or high cholesterol diet (HD). After 4 weeks, Periodic acid-Schiff (PAS) and oil red O staining revealed excessive lipid deposition in the glomeruli of ApoE−/−HD mice, however, significantly suppressed in ApoE−/−/OPN−/−HD mice. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression was lower in the glomeruli of ApoE−/−/OPN−/−HD mice than ApoE−/−HD mice. In vitro study, primary mesangial cells were incubated with recombinant mouse OPN (rmOPN). RmOPN induced LOX-1 mRNA and protein expression in primary mesangial cells. Pre-treatment with an ERK inhibitor suppressed the LOX-1 gene expression induced by rmOPN. These results indicate that OPN contributes to kidney damage in hypercholesterolemia and suggest that inhibition of OPN may provide a potential therapeutic target for the prevention of hypercholesterolemia.
Long Non-coding RNA H19 Inhibits Adipocyte Differentiation of Bone Marrow Mesenchymal Stem Cells through Epigenetic Modulation of Histone Deacetylases
Authors: Huang Yiping , Zheng Yunfei , Jin Chanyuan , Li Xiaobei , Jia Lingfei , Li Weiran 
Published: June 2016

AbstractBone marrow mesenchymal stem cells (BMSCs) exhibit an increased propensity toward adipocyte differentiation accompanied by a reduction in osteogenesis in osteoporotic bone marrow. However, limited knowledge is available concerning the role of long non-coding RNAs (lncRNAs) in the differentiation of BMSCs into adipocytes. In this study, we demonstrated that lncRNA H19 and microRNA-675 (miR-675) derived from H19 were significantly downregulated in BMSCs that were differentiating into adipocytes. Overexpression of H19 and miR-675 inhibited adipogenesis, while knockdown of their endogenous expression accelerated adipogenic differentiation. Mechanistically, we found that miR-675 targeted the 3′ untranslated regions of the histone deacetylase (HDAC) 4–6 transcripts and resulted in deregulation of HDACs 4–6, essential molecules in adipogenesis. In turn, trichostatin A, an HDAC inhibitor, significantly reduced CCCTC-binding factor (CTCF) occupancy in the imprinting control region upstream of the H19 gene locus and subsequently downregulated the expression of H19. These results show that the CTCF/H19/miR-675/HDAC regulatory pathway plays an important role in the commitment of BMSCs into adipocytes.
(-)-SCR1693 Protects against Memory Impairment and Hippocampal Damage in a Chronic Cerebral Hypoperfusion Rat Model
Authors: Zhu Xiaoyin , Tian Jingwei , Sun Songmei , Dong Qiuju , Zhang Fangxi , Zhang Xiumei 
Published: June 2016

AbstractChronic cerebral hypoperfusion (CCH) is one of the most common causes of vascular dementia (VaD) and is recognised as an etiological factor in the development of Alzheimer’s disease (AD). CCH can induce severe cognitive deficits, as assessed by the water maze task, along with neuronal loss in the hippocampus. However, there are currently no effective, approved pharmacological treatments available for VaD. In the present study, we created a rat model of CCH using bilateral common carotid artery occlusion and found that (-)-SCR1693, a novel compound, prevented rats from developing memory deficits and neuronal damage in the hippocampus by rectifying cholinergic dysfunction and decreasing the accumulation of the phospho-tau protein. These results strongly suggest that (-)-SCR1693 has therapeutic potential for the treatment of CCH-induced VaD.
Re-evaluation of EMG-torque relation in chronic stroke using linear electrode array EMG recordings
Authors: Bhadane Minal , Liu Jie , Rymer W. Zev , Zhou Ping , Li Sheng 
Published: June 2016

AbstractThe objective was to re-evaluate the controversial reports of EMG-torque relation between impaired and non-impaired sides using linear electrode array EMG recordings. Ten subjects with chronic stroke performed a series of submaximal isometric elbow flexion tasks. A 20-channel linear array was used to record surface EMG of the biceps brachii muscles from both impaired and non-impaired sides. M-wave recordings for bilateral biceps brachii muscles were also made. Distribution of the slope of the EMG-torque relations for the individual channels showed a quasi-symmetrical “M” shaped pattern. The lowest value corresponded to the innervation zone (IZ) location. The highest value from the slope curve for each side was selected for comparison to minimize the effect of electrode placement and IZ asymmetry. The slope was greater on the impaired side in 4 of 10 subjects. There were a weak correlation between slope ratio and strength ratio and a moderate to high correlation between slope ratio and M-wave ratio between two sides. These findings suggest that the EMG-torque relations are likely mediated and influenced by multiple factors. Our findings emphasize the importance of electrode placement and suggest the primary role of peripheral adaptive changes in the EMG-torque relations in chronic stroke.
High Fat Diets Induce Colonic Epithelial Cell Stress and Inflammation that is Reversed by IL-22
Authors: Gulhane Max , Murray Lydia , Lourie Rohan , Tong Hui , Sheng Yong H. , Wang Ran , Kang Alicia , Schreiber Veronika , Wong Kuan Yau , Magor Graham , Denman Stuart , Begun Jakob , Florin Timothy H. , Perkins Andrew , Cuív Páraic Ó. , McGuckin Michael A. , Hasnain Sumaira Z. 
Published: June 2016

AbstractProlonged high fat diets (HFD) induce low-grade chronic intestinal inflammation in mice, and diets high in saturated fat are a risk factor for the development of human inflammatory bowel diseases. We hypothesized that HFD-induced endoplasmic reticulum (ER)/oxidative stress occur in intestinal secretory goblet cells, triggering inflammatory signaling and reducing synthesis/secretion of proteins that form the protective mucus barrier. In cultured intestinal cells non-esterified long-chain saturated fatty acids directly increased oxidative/ER stress leading to protein misfolding. A prolonged HFD elevated the intestinal inflammatory cytokine signature, alongside compromised mucosal barrier integrity with a decrease in goblet cell differentiation and Muc2, a loss in the tight junction protein, claudin-1 and increased serum endotoxin levels. In Winnie mice, that develop spontaneous colitis, HFD-feeding increased ER stress, further compromised the mucosal barrier and increased the severity of colitis. In obese mice IL-22 reduced ER/oxidative stress and improved the integrity of the mucosal barrier, and reversed microbial changes associated with obesity with an increase in Akkermansia muciniphila. Consistent with epidemiological studies, our experiments suggest that HFDs are likely to impair intestinal barrier function, particularly in early life, which partially involves direct effects of free-fatty acids on intestinal cells, and this can be reversed by IL-22 therapy.
Integrative Network-based Analysis of Magnetic Resonance Spectroscopy and Genome Wide Expression in Glioblastoma multiforme
Authors: Heiland Dieter Henrik , Mader Irina , Schlosser Pascal , Pfeifer Dietmar , Carro Maria Stella , Lange Thomas , Schwarzwald Ralf , Vasilikos Ioannis , Urbach Horst , Weyerbrock Astrid 
Published: June 2016

AbstractThe goal of this study was to identify correlations between metabolites from proton MR spectroscopy and genetic pathway activity in glioblastoma multiforme (GBM). Twenty patients with primary GBM were analysed by short echo-time chemical shift imaging and genome-wide expression analyses. Weighed Gene Co-Expression Analysis was used for an integrative analysis of imaging and genetic data. N-acetylaspartate, normalised to the contralateral healthy side (nNAA), was significantly correlated to oligodendrocytic and neural development. For normalised creatine (nCr), a group with low nCr was linked to the mesenchymal subtype, while high nCr could be assigned to the proneural subtype. Moreover, clustering of normalised glutamine and glutamate (nGlx) revealed two groups, one with high nGlx being attributed to the neural subtype and one with low nGlx associated with the classical subtype. Hence, the metabolites nNAA, nCr and nGlx correlate with a specific gene expression pattern reflecting the previously described subtypes of GBM. Moreover high nNAA was associated with better clinical prognosis, whereas patients with lower nNAA revealed a shorter progression-free survival (PFS).
Next-generation sequencing-based molecular diagnosis of neonatal hypotonia in Chinese Population
Authors: Wang Yan , Peng Wei , Guo Hong-Yan , Li Hui , Tian Jie , Shi Yu-Jing , Yang Xiao , Yang Yao , Zhang Wan-Qiao , Liu Xin , Liu Guan-Nan , Deng Tao , Sun Yi-Min , Xing Wan-li , Cheng Jing , Feng Zhi-Chun 
Published: June 2016

AbstractNeonatal hypotonia is extremely challenging to diagnose because numerous disorders present similar clinical manifestations. Two panels for diagnosing neonatal hypotonia were developed, which enriches 35 genes corresponding to 61 neonatal hypotonia-related disorders. A cohort of 214 neonates with hypotonia was recruited from 2012 to 2014 in China for this study. Of these subjects, twenty-eight neonates with hypotonia were eliminated according to exclusion criteria and 97 were confirmed using traditional detection methods. The clinical diagnoses of the remaining 89 neonates with hypotonia were approached by targeted next-generation sequencing (NGS). Among the 89 tested neonates, 25 potentially pathogenic variants in nine genes (RYR1, MECP2, MUT, CDKL5, MPZ, PMM2, MTM1, LAMA2 and DMPK) were identified in 22 patients. Six of these pathogenic variants were novel. Of the 186 neonates with hypotonia, we identified the genetic causes for 117 neonates by the traditional detection methods and targeted NGS, achieving a high solving rate of 62.9%. In addition, we found seven neonates with RETT syndrome carrying five mutations, thus expanding the mutation profiles in Chinese neonates with hypotonia. Our study highlights the utility of comprehensive molecular genetic testing, which provides the advantage of speed and diagnostic specificity without invasive procedures.
Disentangling the autism−anxiety overlap: fMRI of reward processing in a community-based longitudinal study
Authors: Mikita N , Simonoff E , Pine D S , Goodman R , Artiges E , Banaschewski T , Bokde A L , Bromberg U , Büchel C , Cattrell A , Conrod P J , Desrivières S , Flor H , Frouin V , Gallinat J , Garavan H , Heinz A , Ittermann B , Jurk S , Martinot J L , Paillère Martinot M L , Nees F , Papadopoulos Orfanos D , Paus T , Poustka L , Smolka M N , Walter H , Whelan R , Schumann G , Stringaris A 
Published: June 2016

AbstractUp to 40% of youth with autism spectrum disorder (ASD) also suffer from anxiety, and this comorbidity is linked with significant functional impairment. However, the mechanisms of this overlap are poorly understood. We investigated the interplay between ASD traits and anxiety during reward processing, known to be affected in ASD, in a community sample of 1472 adolescents (mean age=14.4 years) who performed a modified monetary incentive delay task as part of the Imagen project. Blood-oxygen-level dependent (BOLD) responses to reward anticipation and feedback were compared using a 2x2 analysis of variance test (ASD traits: low/high; anxiety symptoms: low/high), controlling for plausible covariates. In addition, we used a longitudinal design to assess whether neural responses during reward processing predicted anxiety at 2-year follow-up. High ASD traits were associated with reduced BOLD responses in dorsal prefrontal regions during reward anticipation and negative feedback. Participants with high anxiety symptoms showed increased lateral prefrontal responses during anticipation, but decreased responses following feedback. Interaction effects revealed that youth with combined ASD traits and anxiety, relative to other youth, showed high right insula activation when anticipating reward, and low right-sided caudate, putamen, medial and lateral prefrontal activations during negative feedback (all clusters PFWE<0.05). BOLD activation patterns in the right dorsal cingulate and right medial frontal gyrus predicted new-onset anxiety in participants with high but not low ASD traits. Our results reveal both quantitatively enhanced and qualitatively distinct neural correlates underlying the comorbidity between ASD traits and anxiety. Specific neural responses during reward processing may represent a risk factor for developing anxiety in ASD youth.
Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders
Authors: Theoharides T C , Tsilioni I , Patel A B , Doyle R 
Published: June 2016

AbstractAutism spectrum disorders (ASDs) affect as many as 1 in 45 children and are characterized by deficits in sociability and communication, as well as stereotypic movements. Many children also show severe anxiety. The lack of distinct pathogenesis and reliable biomarkers hampers the development of effective treatments. As a result, most children with ASD are prescribed psychopharmacologic agents that do not address the core symptoms of ASD. Autoantibodies against brain epitopes in mothers of children with ASD and many such children strongly correlate with allergic symptoms and indicate an aberrant immune response, as well as disruption of the blood–brain barrier (BBB). Recent epidemiological studies have shown a strong statistical correlation between risk for ASD and either maternal or infantile atopic diseases, such as asthma, eczema, food allergies and food intolerance, all of which involve activation of mast cells (MCs). These unique tissue immune cells are located perivascularly in all tissues, including the thalamus and hypothalamus, which regulate emotions. MC-derived inflammatory and vasoactive mediators increase BBB permeability. Expression of the inflammatory molecules interleukin (IL-1β), IL-6, 1 L-17 and tumor necrosis factor (TNF) is increased in the brain, cerebrospinal fluid and serum of some patients with ASD, while NF-kB is activated in brain samples and stimulated peripheral blood immune cells of other patients; however, these molecules are not specific. Instead the peptide neurotensin is uniquely elevated in the serum of children with ASD, as is corticotropin-releasing hormone, secreted from the hypothalamus under stress. Both peptides trigger MC to release IL-6 and TNF, which in turn, stimulate microglia proliferation and activation, leading to disruption of neuronal connectivity. MC-derived IL-6 and TGFβ induce maturation of Th17 cells and MCs also secrete IL-17, which is increased in ASD. Serum IL-6 and TNF may define an ASD subgroup that benefits most from treatment with the natural flavonoid luteolin. Atopic diseases may create a phenotype susceptible to ASD and formulations targeting focal inflammation of the brain could have great promise in the treatment of ASD.
Fast active islanding detection method based on second harmonic drifting for inverter‐based distributed generation
Authors: Emadi Ali , Afrakhte Hosein , Sadeh Javad 
Published: June 2016

Voltage drifting islanding detection methods (IDMs) force the voltage at point of common coupling (PCC) to move outside the appropriate limits, so that under/over voltage protection disconnects distributed generation (DG) units. This kind of IDMs does not possess the advantage of keeping micro‐grid energized after islanding occurrence. There are active IDMs without forcing the islanded micro‐grid to lose its stable operation but they degrade the power quality because of perturbation injection. In this study, an active IDM is proposed which makes the second harmonic of PCC voltage drift suddenly after islanding occurrence and pass a predefined threshold value without affecting the fundamental component. When islanding is detected the method is deactivated and the voltage and frequency remain in expected limits in the conditions of power balance. Another advantage of the proposed method is that it decreases the second harmonic of PCC voltage in grid‐connected mode and improves the power quality of system unlike other active IDMs. The UL 1741 test results show that the proposed method detects islanding occurrence in a multi‐inverter system in <100 ms. Also, the correct performance of the proposed method has been shown for non‐islanding conditions. The paper simulations are performed using PSCAD/EMTDC software.