bluuebunny/crossref_metadata_2025_split huggingface dataset:
Revisiting lake sediment budgets: How the calculation of lake lifetime is strongly data and method dependent
Authors: Lemma Hanibal , Admasu Teshager , Dessie Mekete , Fentie Derbew , Deckers Jozef , Frankl Amaury , Poesen Jean , Adgo Enyew , Nyssen Jan 
Published: September 2017

AbstractLake sedimentation has a fundamental impact on lake lifetime. In this paper, we show how sensitive calculation of the latter is to the quality of data available and assumptions made during analysis. Based on the collection of a large new dataset, we quantify the sediment masses (1) mobilized on the hillslopes draining towards Lake Tana (Ethiopia), (2) stored in the floodplains, (3) transported into the lake, (4) deposited in the lake and (5) delivered out from the lake so as to establish a sediment budget. In 2012–2013, suspended sediment concentration (SSC) and discharge measurements were made at 13 monitoring stations, including two lake outlets. Altogether, 4635 SSC samples were collected and sediment rating curves that account for land cover conditions and rainfall seasonality were established for the 11 river stations, and mean monthly SSC was calculated for the outlets. Effects of the floodplain on rivers' sediment yield (SY) were investigated using measurements at both sides of the floodplains. SY from ungauged rivers was assessed using a model that includes catchment area and rainfall, whereas bedload and direct sediment input from lake shores were estimated. As a result, the gross annual SY was c. 39.55 (± 0.15) Mt, dominantly from Gilgel Abay and Gumara Rivers. The 2.57 (± 0.17) Mt sediment deposited in floodplains indicate that the floodplains serve as an important sediment sink. Moreover, annually c. 1.09 Mt of sediment leaves the lake through the two outlets. Annual sediment deposition in the lake was c. 36.97 (± 0.22) Mt and organic matter accumulation was 2.15 Mt, with a mean sediment trapping efficiency of 97%. Furthermore, SSC and SY are generally higher at the beginning of the rainy season because soils in cultivated fields are bare and loose due to frequent ploughing and seedbed preparation. Later in the season, increased crop and vegetation cover lead to a decrease in sediment production. Based on the established sediment budget with average rainfall, the lifetime of Lake Tana was estimated as 764 to 1032 years, which is shorter than what was anticipated in earlier studies. The sedimentation rate of Lake Tana (11.7 ± 0.1 kg m−2 yr−1) is in line with the sedimentation rates of larger lakes in the world, like Lake Dongting and Lake Kivu. Copyright © 2017 John Wiley & Sons, Ltd.
Analysis of earthworm sublethal toxic responses to atrazine exposure using 1H nuclear magnetic resonance (NMR)-based metabolomics
Authors: Dani Vivek D. , Simpson André J. , Simpson Myrna J. 
Published: September 2017

Abstract

Atrazine toxicity to earthworms is still not fully understood, particularly at sublethal concentrations. Because of the ubiquity of atrazine in the environment, it is imperative to understand the impacts of atrazine presence to soil-dwelling organisms. To examine this in detail, we used 1H nuclear magnetic resonance (NMR)-based metabolomics to elucidate earthworm (Eisenia fetida) responses after 48 h of atrazine exposure in contact tests. Earthworms were exposed to 4 sublethal concentrations of 362.4, 181.2, 90.6, and 45.3 ng/cm2, which correspond to 1/8th, 1/16th, 1/32nd, and 1/64th of the median lethal concentration (LC50) values, respectively. After exposure, polar metabolites were isolated from earthworm tissues and analyzed using 1H NMR spectroscopy. Sublethal atrazine exposure induced a nonmonotonic response with respect to exposure concentration and caused an overall suppression in earthworm metabolism. Maltose, fumarate, malate, threonine/lactate, adenosine-5′-triphosphate (ATP), betaine, scyllo-inositol, glutamate, arginine, and glutamine were the metabolites identified as most sensitive to atrazine exposure. These observed fluctuations in the metabolic profile suggest that atrazine reduced ATP synthesis and negatively impacted the health of earthworms after acute sublethal exposure. Our study also demonstrates the utility of NMR-based metabolomics for the basic assessment of sublethal toxicity, which can then be used for more targeted approaches with other molecular techniques. Environ Toxicol Chem 2018;37:473–480. © 2017 SETAC
Regulation of radial glial process growth by glutamate via mGluR5/TRPC3 and neuregulin/ErbB4
Authors: Louhivuori Lauri M. , Turunen Pauli M. , Louhivuori Verna , Yellapragada Venkatram , Nordström Tommy , Uhlén Per , Åkerman Karl E. 
Published: September 2017

AbstractRadial glial cells play an essential role through their function as guides for neuronal migration during development. Disruption of metabotropic glutamate receptor 5 (mGluR5) function retards the growth of radial glial processes in vitro. Neuregulins (NRG) are activated by proteolytic cleavage and regulate (radial) glial maintenance via ErbB3/ErbB4 receptors. We show here that blocking ErbB4 disrupts radial process extension. Soluble NRG acting on ErbB4 receptors is able to promote radial process extension in particular where process elongation has been impeded by blockade of mGluR5, the nonselective cation channel canonical transient receptor potential 3 (TRPC3), or matrix metalloproteases (MMP). NRG does not restore retarded process growth caused by ErbB4 blockade. Stimulation of muscarinic receptors restores process elongation due to mGluR5 blockade but not that caused by TRPC3, MMP or ErbB4 blockade suggesting that muscarinic receptors can replace mGluR5 with respect to radial process extension. Additionally, NRG/ErbB4 causes Ca2+ mobilization in a population of cells through cooperation with ErbB1 receptors. Our results indicate that mGluR5 promotes radial process growth via NRG activation by a mechanism involving TRPC3 channels and MMPs. Thus neurotransmitters acting on G‐protein coupled receptors could play a central role in the maintenance of the radial glial scaffold through activation of NRG/ErbB4 signaling.
Disconnection of hippocampal networks contributes to memory dysfunction in individuals with temporal lobe epilepsy
Authors: Stoub Travis R. , Chicharro Ada V. , Grote Christopher L. , Kanner Andres M. 
Published: September 2017

AbstractA deficit in declarative memory function is common among individuals with temporal lobe epilepsy. The purpose of this study is to evaluate the relationship between the volume of the hippocampus, entorhinal cortex along with the surrounding parahippocampal white matter and memory performance in those with temporal lobe epilepsy. T1 weighted MRI scans were acquired using a 3‐D pulse sequence in 50 individuals with temporal lobe epilepsy. Hippocampal and entorhinal cortex volumes were derived by manually tracing consecutive coronal slices aligned perpendicular to the long axis of the hippocampus. In addition, parahippocampal white matter volumes were determined using voxel based morphometry. Finally, declarative memory was assessed using immediate and delayed verbal and visual memory tests from the Wechsler Memory Scale third edition. Significant correlations were seen between right and left hippocampal volumes and delayed verbal memory test scores. In addition, left parahippocampal white matter showed positive correlations with immediate and delayed verbal and visual recall. Furthermore, regression models found that the right hippocampus and left parahippocampal white matter were the best predictors of immediate and delayed verbal and visual memory performance. These results show that a decrease in white matter fibers projecting to the hippocampus may cause a disruption of incoming multi‐modal sensory information, contributing to the memory decline seen in individuals with temporal lobe epilepsy.
Close but no cigar: Spatial precision deficits following medial temporal lobe lesions provide novel insight into theoretical models of navigation and memory
Authors: Kolarik Branden S. , Baer Trevor , Shahlaie Kiarash , Yonelinas Andrew P. , Ekstrom Arne D. 
Published: September 2017

AbstractIncreasing evidence suggests that the human hippocampus contributes to a range of different behaviors, including episodic memory, language, short‐term memory, and navigation. A novel theoretical framework, the Precision and Binding Model, accounts for these phenomenon by describing a role for the hippocampus in high‐resolution, complex binding. Other theories like Cognitive Map Theory, in contrast, predict a specific role for the hippocampus in allocentric navigation, while Declarative Memory Theory predicts a specific role in delay‐dependent conscious memory. Navigation provides a unique venue for testing these predictions, with past results from research with humans providing inconsistent findings regarding the role of the human hippocampus in spatial navigation. Here, we tested five patients with lesions primarily restricted to the hippocampus and those extending out into the surrounding medial temporal lobe cortex on a virtual water maze task. Consistent with the Precision and Binding Model, we found partially intact allocentric memory in all patients, with impairments in the spatial precision of their searches for a hidden target. We found similar impairments at both immediate and delayed testing. Our findings are consistent with the Precision and Binding Model of hippocampal function, arguing for its role across domains in high‐resolution, complex binding.Significance StatementRemembering goal locations in one's environment is a critical skill for survival. How this information is represented in the brain is still not fully understood, but is believed to rely in some capacity on structures in the medial temporal lobe. Contradictory findings from studies of both humans and animals have been difficult to reconcile with regard to the role of the MTL, specifically the hippocampus. By assessing impairments observed during navigation to a goal in patients with medial temporal lobe damage we can better understand the role these structures play in such behavior. Utilizing virtual reality and novel analysis techniques, we have more precisely assessed the impact that medial temporal lobe damage has on spatial memory and navigation.
Selective decline of neurotrophin and neurotrophin receptor genes within CA1 pyramidal neurons and hippocampus proper: Correlation with cognitive performance and neuropathology in mild cognitive impairment and Alzheimer's disease
Authors: Ginsberg Stephen D. , Malek‐Ahmadi Michael H. , Alldred Melissa J. , Che Shaoli , Elarova Irina , Chen Yinghua , Jeanneteau Freddy , Kranz Thorsten M. , Chao Moses V , Counts Scott E. , Mufson Elliott J. 
Published: September 2017

AbstractHippocampal CA1 pyramidal neurons, a major component of the medial temporal lobe memory circuit, are selectively vulnerable during the progression of Alzheimer's disease (AD). The cellular mechanism(s) underlying degeneration of these neurons and the relationship to cognitive performance remains largely undefined. Here, we profiled neurotrophin and neurotrophin receptor gene expression within microdissected CA1 neurons along with regional hippocampal dissections from subjects who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI), or AD using laser capture microdissection (LCM), custom‐designed microarray analysis, and qPCR of CA1 subregional dissections. Gene expression levels were correlated with cognitive test scores and AD neuropathology criteria. We found a significant downregulation of several neurotrophin genes (e.g., Gdnf, Ngfb, and Ntf4) in CA1 pyramidal neurons in MCI compared to NCI and AD subjects. In addition, the neurotrophin receptor transcripts TrkB and TrkC were decreased in MCI and AD compared to NCI. Regional hippocampal dissections also revealed select neurotrophic gene dysfunction providing evidence for vulnerability within the hippocampus proper during the progression of dementia. Downregulation of several neurotrophins of the NGF family and cognate neurotrophin receptor (TrkA, TrkB, and TrkC) genes correlated with antemortem cognitive measures including the Mini‐Mental State Exam (MMSE), a composite global cognitive score (GCS), and Episodic, Semantic, and Working Memory, Perceptual Speed, and Visuospatial domains. Significant correlations were found between select neurotrophic expression downregulation and neuritic plaques (NPs) and neurofibrillary tangles (NFTs), but not diffuse plaques (DPs). These data suggest that dysfunction of neurotrophin signaling complexes have profound negative sequelae within vulnerable hippocampal cell types, which play a role in mnemonic and executive dysfunction during the progression of AD.
Bioabsorbable nerve conduits coated with induced pluripotent stem cell‐derived neurospheres enhance axonal regeneration in sciatic nerve defects in aged mice
Authors: Yokoi Takuya , Uemura Takuya , Takamatsu Kiyohito , Shintani Kosuke , Onode Ema , Okada Mitsuhiro , Hidaka Noriaki , Nakamura Hiroaki 
Published: September 2017

AbstractAging influences peripheral nerve regeneration. Nevertheless, most basic research of bioabsorbable nerve conduits including commercial products have been performed in very young animals. Results from these studies may not provide information about axonal regeneration in aged tissue, because young nerve tissue holds sufficient endogenous potential for axonal regeneration. The clinical target age for nerve conduit application is most likely going to increase with a rapidly growing elderly population. In the present study, we examined axonal regeneration after sciatic nerve defects in aged and young mice. 5‐mm sciatic nerve defects in young (6 weeks old) and aged (92 weeks old) mice were reconstructed using nerve conduits (composed of a poly lactide and caprolactone) or autografts. In addition, in aged mice, sciatic nerve defects were reconstructed using nerve conduits coated with mouse induced pluripotent stem cell (iPSc)‐derived neurospheres. Using electrophysiological and histological techniques, we demonstrated axonal regeneration was significantly less effective in aged than in young mice both for nerve conduits and for nerve autografts. However, despite the low regenerative capacity of the peripheral nerve in aged mice, axonal regeneration significantly increased when nerve conduits coated with iPSc‐derived neurospheres, rather than nerve conduits alone, were used. The present study shows that aging negatively affects peripheral nerve regeneration based on nerve conduits in mice. However, axonal regeneration using nerve conduits was improved when supportive iPSc‐derived neurospheres were added in the aged mice. We propose that tissue‐engineered bioabsorbable nerve conduits in combination with iPSc‐derived neurospheres hold therapeutic potential both in young and elderly patients. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 106B: 1752–1758, 2018.
Small‐molecule inhibition of MuRF1 attenuates skeletal muscle atrophy and dysfunction in cardiac cachexia
Authors: Bowen Thomas Scott , Adams Volker , Werner Sarah , Fischer Tina , Vinke Paulien , Brogger Maria Noel , Mangner Norman , Linke Axel , Sehr Peter , Lewis Joe , Labeit Dittmar , Gasch Alexander , Labeit Siegfried 
Published: September 2017

AbstractBackgroundMuscle ring finger 1 (MuRF1) is a muscle‐specific ubiquitin E3 ligase activated during clinical conditions associated with skeletal muscle wasting. Yet, there remains a paucity of therapeutic interventions that directly inhibit MuRF1 function, particularly in vivo. The current study, therefore, developed a novel compound targeting the central coiled coil domain of MuRF1 to inhibit muscle wasting in cardiac cachexia.MethodsWe identified small molecules that interfere with the MuRF1–titin interaction from a 130 000 compound screen based on Alpha Technology. A subset of nine prioritized compounds were synthesized and administrated during conditions of muscle wasting, that is, to C2C12 muscle cells treated with dexamethasone and to mice treated with monocrotaline to induce cardiac cachexia.ResultsThe nine selected compounds inhibited MuRF1–titin complexation with IC50 values <25 μM, of which three were found to also inhibit MuRF1 E3 ligase activity, with one further showing low toxicity on cultured myotubes. This last compound, EMBL chemical core ID#704946, also prevented atrophy in myotubes induced by dexamethasone and attenuated fibre atrophy and contractile dysfunction in mice during cardiac cachexia. Proteomic and western blot analyses showed that stress pathways were attenuated by ID#704946 treatment, including down‐regulation of MuRF1 and normalization of proteins associated with apoptosis (BAX) and protein synthesis (elF2B‐delta). Furthermore, actin ubiquitinylation and proteasome activity was attenuated.ConclusionsWe identified a novel compound directed to MuRF1's central myofibrillar protein recognition domain. This compound attenuated in vivo muscle wasting and contractile dysfunction in cardiac cachexia by protecting de novo protein synthesis and by down‐regulating apoptosis and ubiquitin‐proteasome‐dependent proteolysis.
Comparison of anatomic and non‐anatomic hepatic resection for hepatocellular carcinoma
Authors: Kaibori Masaki , Kon Masanori , Kitawaki Tomoki , Kawaura Takayuki , Hasegawa Kiyoshi , Kokudo Norihiro , Ariizumi Shunichi , Beppu Toru , Ishizu Hiroyuki , Kubo Shoji , Kamiyama Toshiya , Takamura Hiroyuki , Kobayashi Tsuyoshi , Kim Dong‐Sik , Wang Hee Jung , Kim Jong Man , Han Dai Hoon , Park Sang‐Jae , Kang Koo Jeong , Hwang Shin , Roh Younghoon , You Young Kyung , Joh Jae‐Won , Yamamoto Masakazu 
Published: September 2017

AbstractBackgroundThe aim of the present study was to compare the prognostic impact of anatomic resection (AR) versus non‐anatomic resection (NAR) on patient survival after resection of a single hepatocellular carcinoma (HCC).MethodsTo control for confounding variable distributions, a 1‐to‐1 propensity score match was applied to compare the outcomes of AR and NAR. Among 710 patients with a primary, solitary HCC of <5.0 cm in diameter that was resectable by either AR or NAR from 2003 to 2007 in Japan and Korea, 355 patients underwent NAR and 355 underwent AR of at least one section with complete removal of the portal territory containing the tumor.ResultsOverall survival (OS) was better in the AR than NAR group (hazard ratio 1.67, 95% confidence interval 1.28–2.19, P < 0.001) while disease‐free survival showed no significant difference. Significantly fewer patients in the AR than NAR group developed intrahepatic HCC recurrence and multiple intrahepatic recurrences. Patients with poorly differentiated HCC who underwent AR had improved disease‐free survival and OS.ConclusionsAnatomic resection decreases the risk of tumor recurrence and improves OS in patients with a primary, solitary HCC of <5.0 cm in diameter.
Tokyo Guidelines 2018: management strategies for gallbladder drainage in patients with acute cholecystitis (with videos)
Authors: Mori Yasuhisa , Itoi Takao , Baron Todd H. , Takada Tadahiro , Strasberg Steven M. , Pitt Henry A. , Ukai Tomohiko , Shikata Satoru , Noguchi Yoshinori , Teoh Anthony Yuen Bun , Kim Myung‐Hwan , Asbun Horacio J. , Endo Itaru , Yokoe Masamichi , Miura Fumihiko , Okamoto Kohji , Suzuki Kenji , Umezawa Akiko , Iwashita Yukio , Hibi Taizo , Wakabayashi Go , Han Ho‐Seong , Yoon Yoo‐Seok , Choi In‐Seok , Hwang Tsann‐Long , Chen Miin‐Fu , Garden O. James , Singh Harjit , Liau Kui‐Hin , Huang Wayne Shih‐Wei , Gouma Dirk J. , Belli Giulio , Dervenis Christos , de Santibañes Eduardo , Giménez Mariano Eduardo , Windsor John A. , Lau Wan Yee , Cherqui Daniel , Jagannath Palepu , Supe Avinash Nivritti , Liu Keng‐Hao , Su Cheng‐Hsi , Deziel Daniel J. , Chen Xiao‐Ping , Fan Sheung Tat , Ker Chen‐Guo , Jonas Eduard , Padbury Robert , Mukai Shuntaro , Honda Goro , Sugioka Atsushi , Asai Koji , Higuchi Ryota , Wada Keita , Yoshida Masahiro , Mayumi Toshihiko , Hirata Koichi , Sumiyama Yoshinobu , Inui Kazuo , Yamamoto Masakazu 
Published: September 2017

AbstractSince the publication of the Tokyo Guidelines in 2007 and their revision in 2013, appropriate management for acute cholecystitis has been more clearly established. Since the last revision, several manuscripts, especially for alternative endoscopic techniques, have been reported; therefore, additional evaluation and refinement of the 2013 Guidelines is required. We describe a standard drainage method for surgically high‐risk patients with acute cholecystitis and the latest developed endoscopic gallbladder drainage techniques described in the updated Tokyo Guidelines 2018 (TG18). Our study confirmed that percutaneous transhepatic gallbladder drainage should be considered the first alternative to surgical intervention in surgically high‐risk patients with acute cholecystitis. Also, endoscopic transpapillary gallbladder drainage or endoscopic ultrasound‐guided gallbladder drainage can be considered in high‐volume institutes by skilled endoscopists. In the endoscopic transpapillary approach, either endoscopic naso‐gallbladder drainage or gallbladder stenting can be considered for gallbladder drainage. We also introduce special techniques and the latest outcomes of endoscopic ultrasound‐guided gallbladder drainage studies. Free full articles and mobile app of TG18 are available at: http://www.jshbps.jp/modules/en/index.php?content_id=47. Related clinical questions and references are also included.
Evaluation of loading parameters for murine axial tibial loading: Stimulating cortical bone formation while reducing loading duration
Authors: Sun David , Brodt Michael D. , Zannit Heather M. , Holguin Nilsson , Silva Matthew J. 
Published: September 2017

ABSTRACTClassic studies in bone mechanobiology have established the importance of loading parameters on the anabolic response. Most of these early studies were done using loading methods not currently in favor, and using non‐murine species. Our objective was to re‐examine the effects of several loading parameters on the response of cortical bone using the contemporary murine axial tibial compression model. We subjected tibias of 5‐month old, female C57Bl/6 mice to cyclic (4 Hz) mechanical loading and examined bone formation responses using dynamic and static histomorphometry. First, using a reference protocol of 1,200 cycles/day, 5 days/week for 2 weeks, we confirmed the significant influence of peak strain magnitude on periosteal mineralizing surface (Ps.MS/BS) and bone formation rate (Ps.BFR/BS) (p < 0.05, ANOVA). There was a significant induction of periosteal lamellar bone at a lower threshold of approx. −1,000 μϵ and a transition from lamellar‐woven bone near −2,000 μϵ. In contrast, on the endocortical surface, bone formation indices did not exhibit a load magnitude‐dependent response and no incidence of woven bone. Next, we found that reducing daily cycle number from 1,200 to 300 to 60 did not diminish the bone formation response (p > 0.05). On the other hand, reducing the daily frequency of loading from 5 consecutive days/week to 3 alternate days/week significantly diminished the periosteal response, from a loading‐induced increase in Ps.MS/BS of 38% (loaded vs. control) for 5 days/week to only 15% for 3 days/week (p < 0.05). Finally, we determined that reducing the study duration from 2 to 1 weeks of loading did not affect bone formation outcomes. In conclusion, cyclic loading to −1,800 μϵ peak strain, at 4 Hz and 60 cycles/day for 5 consecutive days (1 week) induces an increase in periosteal lamellar bone formation with minimal incidence of woven bone in 5‐month‐old C57Bl/6 female mice. Our results provide a basis for reduction of loading duration (daily cycles and study length) without loss of anabolic effect as measured by dynamic histomorphometry. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:682–691, 2018.