bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular evidence for biochemical diversification of phenolamide biosynthesis in rice plants
Authors: Tanabe Kimiaki , Hojo Yuko , Shinya Tomonori , Galis Ivan 
Published: March 2016

AbstractTwo phenolamides (PAs), p‐coumaroylputrescine and feruloylputrescine strongly accumulate in rice (Oryza sativa cv. Nipponbare) leaves subjected to attack of chewing and sucking herbivores. Here we identified and characterized in vitro three novel rice genes that mediated coumaroyl‐CoA/feruloyl‐CoA conjugation to polyamines, putrescine and agmatine. Interestingly, two genes were highly specific for their polyamine substrates, encoding putrescine N‐hydroxycinnamoyltransferase and agmatine N‐hydroxycinnamoyltransferase, while the third enzyme could use both polyamines and it was therefore annotated as putrescine/agmatine N‐hydroxycinnamoyltransferase. All genes were preferentially expressed in rice roots and developing flowers, and in addition, the putrescine/agmatine N‐hydroxycinnamoyltransferase transcripts were strongly induced by wounding in the young rice leaves. Because the wound response of this gene was only partially suppressed in the jasmonoyl‐L‐isoleucine deficient plants (Osjar1), it suggests that its upregulation (as well as inducible PAs in rice) may be largely independent of jasmonoyl‐L‐isoleucine signaling pathway. The finding of three closely related genes with a similar and/or overlapping activity in PA biosynthesis provides another striking example of rapid diversification of plant metabolism in response to environmental stresses in nature.
Lipidomic profiling analysis reveals the dynamics of phospholipid molecules in Arabidopsis thaliana seedling growth
Authors: Wang Yi‐Sheng , Yao Hong‐Yan , Xue Hong‐Wei 
Published: March 2016

AbstractHigh‐throughput lipidomic profiling provides a sensitive approach for discovering minor lipid species. By using an advance in electrospray ionization tandem mass spectrometry, a large set of phospholipid molecular species (126 species) with high resolution were identified from Arabidopsis seedling; of them 31 species are newly identified (16 are unique in plants), including 13 species of phosphatidic acid (PA), nine phosphatidylcholine, six phosphatidylinositol and three phosphatidylserine. Further analysis of the lipidomic profile reveals dynamics of phospholipids and distinct species alterations during seedling development. PA molecules are found at the lowest levels in imbibition and follow an increasing trend during seedling growth, while phosphatidylethanolamine (PE) molecules show the opposite pattern with highest levels at imbibition and a general decreasing trend at later stages. Of PA molecular species, 34:2‐, 34:3‐, 36:4‐, 36:5‐, 38:3‐ and 38:4‐PA increase during radicle emergence, and 34:2‐ and 34:3‐PA reach highest levels during hypocotyl and cotyledon emergence from the seed coat. Conversely, molecular species of PE show higher levels in imbibition and decrease in later stages. These results suggest the crucial roles of specific molecular species and homeostasis of phospholipid molecules in seedling growth and provide insights into the mechanisms of how phospholipid molecules are involved in regulating plant development.
Neuropeptide Y (NPY) in cerebrospinal fluid from patients with Huntington's Disease: increased NPY levels and differential degradation of the NPY1–30 fragment
Authors: Wagner Leona , Björkqvist Maria , Lundh Sofia Hult , Wolf Raik , Börgel Arne , Schlenzig Dagmar , Ludwig Hans‐Henning , Rahfeld Jens‐Ulrich , Leavitt Blair , Demuth Hans‐Ulrich , Petersén Åsa , von Hörsten Stephan 
Published: March 2016

AbstractHuntington's disease (HD) is an inherited and fatal polyglutamine neurodegenerative disorder caused by an expansion of the CAG triplet repeat coding region within the HD gene. Progressive dysfunction and loss of striatal GABAergic medium spiny neurons (MSNs) may account for some of the characteristic symptoms in HD patients. Interestingly, in HD, MSNs expressing neuropeptide Y (NPY) are spared and their numbers is even up‐regulated in HD patients. Consistent with this, we report here on increased immuno‐linked NPY (IL‐NPY) levels in human cerebrospinal fluid (hCSF) from HD patients (Control n = 10; early HD n = 9; mid HD n = 11). As this antibody‐based detection of NPY may provide false positive differences as a result of the antibody‐based detections of only fragments of NPY, the initial finding was validated by investigating the proteolytic stability of NPY in hCSF using matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry (MALDI‐TOF‐MS) and selective inhibitors. A comparison between resulting NPY‐fragments and detailed epitope analysis verified significant differences in IL‐NPY1–36/3–36 and NPY1–30 levels between HD patients and control subjects with no significant differences between early vs mid HD cases. Ex vivo degradomics analysis demonstrated that NPY is initially degraded to NPY1–30 by cathepsin D in both HD patients and control subjects. Yet, NPY1–30 is then further differentially hydrolyzed by thimet oligopeptidase (TOP) in HD patients and by neprilysin (NEP) in control subjects. Furthermore, altered hCSF TOP‐inhibitor Dynorphin A1–13 (Dyn‐A1–13) and TOP‐substrate Dyn‐A1–8 levels indicate an impaired Dyn‐A‐TOP network in HD patients. Thus, we conclude that elevated IL‐NPY‐levels in conjunction with TOP‐/NEP‐activity/protein as well as Dyn‐A1–13‐peptide levels may serve as a potential biomarker in human CSF of HD.
imageHuntington's disease (HD) patients' cerebrospinal fluid (CSF) exhibits higher neuropeptide Y (NPY) levels. Further degradomics studies show that CSF‐NPY is initially degraded to NPY1‐30 by Cathepsin D. The NPY1‐30 fragment is then differentially degraded in HD vs control involving Neprilysin (NEP), Thimet Oligopeptidase (TOP), and TOP‐Dynorphin‐A network. Together, these findings may help in search for HD biomarkers.
Physiological functions and pathobiology of TDP‐43 and FUS/TLS proteins
Authors: Ratti Antonia , Buratti Emanuele 
Published: March 2016

AbstractThe multiple roles played by RNA binding proteins in neurodegeneration have become apparent following the discovery of TAR DNA binding protein 43 kDa (TDP‐43) and fused in sarcoma/translocated in liposarcoma (FUS/TLS) involvement in amyotrophic lateral sclerosis and frontotemporal lobar dementia. In these two diseases, the majority of patients display the presence of aggregated forms of one of these proteins in their brains. The study of their functional properties currently represents a very promising target for developing the effective therapeutic options that are still lacking. This aim, however, must be preceded by an accurate evaluation of TDP‐43 and FUS/TLS biological functions, both in physiological and disease conditions. Recent findings have uncovered several aspects of RNA metabolism that can be affected by misregulation of these two proteins. Progress has also been made in starting to understand how the aggregation of these proteins occurs and spreads from cell to cell. The aim of this review will be to provide a general overview of TDP‐43 and FUS/TLS proteins and to highlight their physiological functions. At present, the emerging picture is that TDP‐43 and FUS/TLS control several aspects of an mRNA's life, but they can also participate in DNA repair processes and in non‐coding RNA metabolism. Although their regulatory activities are similar, they regulate mainly distinct RNA targets and show different pathogenetic mechanisms in amyotrophic lateral sclerosis/frontotemporal lobar dementia diseases. The identification of key events in these processes represents today the best chance of finding targetable options for therapeutic approaches that might actually make a difference at the clinical level.
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The two major RNA Binding Proteins involved in Amyotrophic Lateral Sclerosisi and Frontotemporal Dementia are TDP‐43 and FUST/TLS. Both proteins are involved in regulating all aspects of RNA and RNA life cycle within neurons, from transcription, processing, and transport/stability to the formation of cytoplasmic and nuclear stress granules. For this reason, the aberrant aggregation of these factors during disease can impair multiple RNA metabolic pathways and eventually lead to neuronal death/inactivation. The purpose of this review is to provide an up‐to‐date perspective on what we know about this issue at the molecular level.This article is part of the Frontotemporal Dementia special issue.
Muscle biopsies from human muscle diseases with myopathic pathology reveal common alterations in mitochondrial function
Authors: Sunitha Balaraju , Gayathri Narayanappa , Kumar Manish , Keshava Prasad Thottethodi Subrahmanya , Nalini Atchayaram , Padmanabhan Balasundaram , Srinivas Bharath Muchukunte Mukunda 
Published: March 2016

AbstractMuscle diseases are clinically and genetically heterogeneous and manifest as dystrophic, inflammatory and myopathic pathologies, among others. Our previous study on the cardiotoxin mouse model of myodegeneration and inflammation linked muscle pathology with mitochondrial damage and oxidative stress. In this study, we investigated whether human muscle diseases display mitochondrial changes. Muscle biopsies from muscle disease patients, represented by dysferlinopathy (dysfy) (dystrophic pathology; n = 43), polymyositis (PM) (inflammatory pathology; n = 24), and distal myopathy with rimmed vacuoles (DMRV) (distal myopathy; n = 31) were analyzed. Mitochondrial damage (ragged blue and COX‐deficient fibers) was revealed in dysfy, PM, and DMRV cases by enzyme histochemistry (SDH and COX‐SDH), electron microscopy (vacuolation and altered cristae) and biochemical assays (significantly increased ADP/ATP ratio). Proteomic analysis of muscle mitochondria from all three muscle diseases by isobaric tag for relative and absolute quantitation labeling and liquid chromatography‐tandem mass spectrometry (LC‐MS/MS) analysis demonstrated down‐regulation of electron transport chain (ETC) complex subunits, assembly factors and Krebs cycle enzymes. Interestingly, 80 of the under‐expressed proteins were common among the three pathologies. Assay of ETC and Krebs cycle enzyme activities validated the MS data. Mitochondrial proteins from muscle pathologies also displayed higher tryptophan (Trp) oxidation and the same was corroborated in the cardiotoxin model. Molecular modeling predicted Trp oxidation to alter the local structure of mitochondrial proteins. Our data highlight mitochondrial alterations in muscle pathologies, represented by morphological changes, altered mitochondrial proteome and protein oxidation, thereby establishing the role of mitochondrial damage in human muscle diseases.
imageWe investigated whether human muscle diseases display mitochondrial changes. Muscle biopsies from dysferlinopathy (Dysfy), polymyositis (PM), and distal myopathy with rimmed vacuoles (DMRV) displayed morphological and biochemical evidences of mitochondrial dysfunction. Proteomic analysis revealed down‐regulation of electron transport chain (ETC) subunits, assembly factors, and tricarboxylic acid (TCA) cycle enzymes, with 80 proteins common among the three pathologies. Mitochondrial proteins from muscle pathologies also displayed higher Trp oxidation that could alter the local structure.Cover image for this issue: doi: 10.1111/jnc.13324.
Clove bud (Syzygium aromaticum) improved blood and hepatic antioxidant indices in laying hens receiving low n‐6 to n‐3 ratios
Authors: Rahman Alizadeh M. , Mahdavi A. H. , Rahmani H. R. , Jahanian E. 
Published: March 2016

SummaryThis study was carried out to investigate the effects of different levels of clove bud (Syzygium aromaticum) powder and vitamin E on serum lipid profile, enzyme activities and antioxidant indices, as well as hepatic biochemical and histological alterations in laying hens receiving different n‐6 to n‐3 ratios. A total of 160 laying hens, 43 weeks of age, were allotted to 8 experimental diets with 5 cages of 4 birds each. Dietary treatments consisted of two ratios of n‐6 to n‐3 (16.71 and 2.35), three levels of clove bud (0.0, 2.0 and 4.0 g/kg) and a high vitamin E level (200 mg/kg, as a positive control in each level of n‐6 to n‐3 ratio) in a 2 × 4 factorial arrangement during 70 days of the experiment. Results showed that a decline in the n‐6 to n‐3 ratio led to a reduction in serum cholesterol concentration (p < 0.05) and an increase in serum HDL content (p < 0.05). Additionally, decreasing n‐6 to n‐3 ratio and increasing clove bud level caused a remarkable decline in serum aspartate aminotransferase (p < 0.05 and p < 0.001) and alanine aminotransferase (p < 0.05 and p < 0.05) enzyme activities. Furthermore, total antioxidant capacity (p < 0.05 and p < 0.001) as well as serum vitamin E concentration (p < 0.05 and p < 0.001) was decreased and enhanced by low n‐6 to n‐3 ratio diets (LRD) and clove bud powder respectively. Decreasing the n‐6 to n‐3 ratio lowered hepatic lipid (p < 0.05) and glycogen contents (p < 0.01) as well as tissue integrity (p < 0.05), and raised liver MDA concentration (p < 0.001), markedly. Nevertheless, increments in clove bud content led to a reduction (p < 0.01) in liver relative weight (p < 0.05) and hepatic fat vacuole numbers. In general, the best synergistic responses on modulating of blood lipids and serum enzyme activities were observed when the highest level of clove bud was supplemented in the diets with low n‐6 to n‐3 ratio. Likewise, antioxidant indices were improved by administration of dietary clove bud powder although feeding fish oil was observed to elevate the susceptibility of blood and hepatocytes to lipid peroxidation.
Dry matter and digesta particle size gradients along the goat digestive tract on grass and browse diets
Authors: Clauss M. , Fritz J. , Tschuor A. , Braun U. , Hummel J. , Codron D. 
Published: March 2016

SummaryPhysical properties of the digesta vary along the ruminant digestive tract. They also vary within the forestomach, leading to varying degrees of rumen contents stratification in ‘moose‐type’ (browsing) and ‘cattle‐type’ (intermediate and grazing) ruminants. We investigated the dry matter concentration (DM) and the mean digesta particle size (MPS) within the forestomach and along the digestive tract in 10 goats fed grass hay or dried browse after a standardized 12‐h fast, euthanasia and freezing in the natural position. In all animals, irrespective of diet, DM showed a peak in the omasum and an increase from caecum via colon towards the faeces and a decrease in MPS between the reticulum and the omasum. Both patterns are typical for ruminants in general. In the forestomach, there was little systematic difference between more cranial and more caudal locations (‘horizontal stratification’), with the possible exception of large particle segregation in the dorsal rumen blindsac on the grass diet. In contrast, the typical (vertical) contents stratification was evident for DM (with drier contents dorsally) and, to a lower degree, for MPS (with larger particles dorsally). Although evident in both groups, this stratification was more pronounced on the grass diet. The results support the interpretation that differences in rumen contents stratification between ruminants are mainly an effect of species‐specific physiology, but can be enhanced due to the diet consumed.
Organic aggregates formed by benthopleustophyte brown algaAcinetospora crinita(Acinetosporaceae, Ectocarpales)
Authors: Giani Michele , Sartoni Gianfranco , Nuccio Caterina , Berto Daniela , Ferrari Carla Rita , Najdek Mirjana , Sist Paola , Urbani Ranieri 
Published: March 2016

This work presents the elemental, polysaccharide, and fatty acid compositions of benthic aggregates formed by the filamentous brown algaAcinetospora crinita, which are widely spread on the rocky bottoms of the Mediterranean Sea. The aggregates can be characterized as mineralized centers in which regeneration of nutrients and recycling of dissolved organic matter actively occur and favor the development of an abundant phytoplankton community. Analyses of the stable isotopes of C and N display their marine origin and could provide evidence of the processes that occur inside/outside of the aggregates. The monosaccharide compositions of Adriatic and Tyrrhenian mucilages produced by brown algaA. crinitawere quite similar. In particular, the Adriatic sample compositions resembled the average composition of the Tyrrhenian high molecular weight exopolymers, and the observed differences could be ascribed to different degradation stages. The fatty acid patterns found for the aggregates were similar to those observed in the isolatedA. crinitaalgae with variable contributions from embedded diatom species. The bacterial contribution to the fatty acid pool was quite low, most likely due to the known poor conditions for their heterotrophic growth.
Decreased expression of E‐cadherin by Porphyromonas gingivalis‐lipopolysaccharide attenuates epithelial barrier function
Authors: Abe‐Yutori M. , Chikazawa T. , Shibasaki K. , Murakami S. 
Published: March 2016

Background and ObjectiveThe gingival epithelium is a first line of defense against bacterial challenge. E‐cadherin (E‐cad) plays an important role in cell–cell adhesion as a barrier in the epithelium. Recently, a decrease in the expression of E‐cad has been observed in inflamed gingival tissue. The aims of this study were to clarify the changes in E‐cad expression and barrier function in human gingival epithelial cells stimulated with Porphyromonas gingivalis‐lipopolysaccharide (P. gingivalis‐LPS) and to evaluate the influence of these changes on the inflammatory reaction. Furthermore, to clarify the mechanism of the E‐cad changes induced by P. gingivalis‐LPS, we focused on reactive oxygen species (ROS) that are reported to induce a decrease in E‐cad expression.Material and Methods: Human gingival epithelial cells were incubated in Humedia‐KG2 in the presence or absence of P. gingivalis‐LPS and antioxidants to analyze ROS involvement in P. gingivalis‐LPS‐induced E‐cad changes. E‐cad protein expression was analyzed by immunofluorescence staining. To investigate barrier function and inflammatory changes, we performed transport and cytokine assays using gingival epithelial cells and macrophages co‐culture model in transwell plates. Medium containing 10 μg/mL P. gingivalis‐LPS (transport substance) was added to the upper compartment, which harvested gingival epithelial cells, and medium without P. gingivalis‐LPS was added to the lower compartment, which harvested macrophages. In the transport assay, P. gingivalis‐LPS penetration was analyzed using the Limulus amebocyte lysate test. In the cytokine assay, we examined the change in tumor necrosis factor‐α (TNF‐α) production from the macrophages in the lower compartment using enzyme‐linked immunosorbent assay.ResultsExpression of E‐cad in human gingival epithelial cells was decreased by P. gingivalis‐LPS, and the decrease in E‐cad accelerated the penetration of P. gingivalis‐LPS through the monolayer. In addition, the concentration of TNF‐α was higher under the E‐cad reduced monolayer. Antioxidants, particularly vitamin E and l‐ascorbic acid 2‐phosphate magnesium salt, inhibited the decrease in E‐cad expression, penetration of P. gingivalis‐LPS and increase in TNF‐α.ConclusionThese results suggest that the decrease in E‐cad caused by P. gingivalis‐LPS leads to destruction of the epithelial barrier function in human gingival epithelial cells, and finally accelerates the inflammatory reaction under the barrier. Antioxidants, particularly vitamin E and l‐ascorbic acid 2‐phosphate magnesium salt, may restore the impaired function by scavenging ROS, which are related to the decrease in E‐cad expression by P. gingivalis‐LPS.
High levels of heavy metal accumulation in dental calculus of smokers: a pilot inductively coupled plasma mass spectrometry study
Authors: Yaprak E. , Yolcubal İ. , Sinanoğlu A. , Doğrul‐Demiray A. , Guzeldemir‐Akcakanat E. , Marakoğlu İ. 
Published: March 2016

Background and ObjectiveVarious trace elements, including toxic heavy metals, may exist in dental calculus. However, the effect of environmental factors on heavy metal composition of dental calculus is unknown. Smoking is a major environmental source for chronic toxic heavy metal exposition. The aim of this study is to compare toxic heavy metal accumulation levels in supragingival dental calculus of smokers and non‐smokers.Material and MethodsA total of 29 supragingival dental calculus samples were obtained from non‐smoker (n = 14) and smoker (n = 15) individuals. Subjects with a probability of occupational exposure were excluded from the study. Samples were analyzed by inductively coupled plasma mass spectrometry in terms of 26 metals and metalloids, including toxic heavy metals.ResultsToxic heavy metals, arsenic (p < 0.05), cadmium (p < 0.05), lead (p < 0.01), manganese (p < 0.01) and vanadium (p < 0.01) levels were significantly higher in smokers than non‐smokers. The levels of other examined elements were similar in both groups (p > 0.05).ConclusionWithin the limitations of this study, it can be concluded that the elementary composition of dental calculus may be affected by environmental factors such as tobacco smoke. Therefore, dental calculus may be utilized as a non‐invasive diagnostic biological material for monitoring chronic oral heavy metal exposition. However, further studies are required to evaluate its diagnostic potential.
Hypoxia‐inducible factor‐1α inhibits interleukin‐6 and ‐8 production in gingival epithelial cells during hypoxia
Authors: Takedachi M. , Iyama M. , Sawada K. , Mori K. , Yamamoto S. , Morimoto C. , Yanagita M. , Murakami S. 
Published: March 2016

Background and ObjectiveHypoxia has been widely studied in inflammatory diseases as it can modulate the inflammatory response, mainly via the hypoxia‐inducible factor (HIF). However, little is known about the effects of hypoxia and the role of HIF in the inflammatory responses to periodontitis.In this study, we focused on the gingival epithelium that is exposed to relatively low levels of oxygen. We investigated whether hypoxic conditions have an impact on inflammatory responses in human gingival epithelial cells (HGECs).Material and MethodsPimonidazole HCl, which accumulates in hypoxic cells, was administered intraperitoneally to C57BL/6 mice with or without Porphyromonas gingivalis infection. Immunohistochemistry was then performed to detect the hypoxic cells in periodontal tissue. Immortalized HGECs were cultured under hypoxic conditions with or without interleukin (IL)‐1β, and the expression levels of IL‐6 and IL‐8 were measured by real‐time reverse transcription–polymerase chain reaction and enzyme‐linked immunosorbent assay. HIF‐1α expression was detected by western blotting. The DNA‐binding activity of HIF‐1α was determined by a DNA‐binding enzyme‐linked immunosorbent assay. The involvement of HIF‐1α in the hypoxic response was examined by transfection with HIF‐1α siRNA.ResultsImmunohistochemistry revealed pimonidazole HCl accumulation in the gingival epithelium of both normal and P. gingivalis‐infected mice, with a slightly stronger signal in the P. gingivalis‐infected mice than in the normal mice. The IL‐1β‐induced IL‐6 and IL‐8 production by HGECs was suppressed under hypoxic conditions. HIF‐1α accumulated during hypoxia, and this accumulation was further enhanced by IL‐1β treatment. The hypoxia‐dependent suppression of IL‐6 and IL‐8 expression was reversed by treating the cells with HIF‐1α siRNA.ConclusionOur results suggest that the gingival epithelium is exposed to low oxygen tension in periodontal tissue and that this hypoxic condition modulates the local inflammatory response of gingival epithelial cells in an HIF‐1α‐dependent manner.