bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term Effects of Cholestatic Liver Disease in Childhood on Neuropsychological Outcomes and Neurochemistry
Authors: Talcott Joel B. , Beath Sue V. , Patel Tulpesh , Griffiths Gareth , Kelly Deirdre A. 
Published: June 2019

ABSTRACTObjectives:Children with liver disease have increased risk of long‐term cognitive deficits. We differentiated between the effects of chronic liver disease from that associated with transplantation by recruiting children with cholestatic liver disease (CLD) with and without transplantation.Methods:Psychometric measures and magnetic resonance spectroscopy were obtained for 3 groups of children: stable liver disease without transplantation; CLD from birth with transplantation; and individuals healthy to 18 months of age, before transplantation for acute liver failure.Results:Cognitive outcomes between children with different disease histories were significantly associated with the duration of liver disease but not the effects of transplantation, including that of immunosuppression. Lower intellectual ability was most frequently observed in the CLD group, whereas all of the acute liver failure group scored within the normal range. Myoinositol and glutamate/glutamine concentrations in cortex were significantly associated with disease duration across the cohort. Neurometabolite profiles in stable liver disease were consistent with subclinical encephalopathy. Impaired growth in early childhood was associated with later cognitive performance.Conclusion:Children with prolonged liver disease had the poorest cognitive outcomes despite successful transplantation, suggesting that prolonged cholestasis before transplantation adversely affects neurodevelopment, and reinforces the need for timely interventions.
Correlates of Gut Function in Children Hospitalized for Severe Acute Malnutrition, a Cross‐sectional Study in Uganda
Authors: Lanyero Betty , Grenov Benedikte , Barungi Nicolette N. , Namusoke Hanifa , Michaelsen Kim F. , Mupere Ezekiel , Mølgaard Christian , Jiang Pingping , Frøkiær Hanne , Wiese Maria , Muhammed Musemma K. , Pesu Hannah , Nielsen Dennis S. , Friis Henrik , Rytter Maren JH. , Christensen Vibeke B. 
Published: June 2019

ABSTRACTObjective:Children with severe acute malnutrition (SAM) may have impaired intestinal function, which can result in malabsorption, diarrhoea, and poor growth. This study evaluated the gut function of children with SAM using fecal and blood biomarkers and assessed their correlates.Methods:A cross‐sectional study, nested in a randomized trial (www.isrctn.com, ISRCTN 16454889), was conducted at Mulago hospital, Uganda among subgroups of 400 children with complicated SAM and 30 community controls. Gut function was evaluated by 5 biomarkers: plasma citrulline, fecal myeloperoxidase and fecal neopterin, bacterially derived 16S rRNA gene and internal transcribed Spacer region (ITS) specific for Candida spp. in blood.Results:Compared with controls, children with SAM had lower median plasma citrulline (5.14 vs 27.4 μmol/L, P < 0.001), higher median fecal myeloperoxidase (18083 vs 7482 ng/mL, P = 0.001), and fecal neopterin (541 vs 210 nmol/L, P < 0.001). A higher blood concentration of 16S rRNA gene copy numbers was observed among children with SAM (95 vs 28 copies/μl, P = 0.05), whereas there was no difference in the blood concentration of Candida‐specific ITS fragment.Among those with SAM, plasma citrulline was lower in children with edema, diarrhoea, dermatosis, and plasma C‐reactive protein (CRP) >10 mg/L. Fecal neopterin was positively correlated with symptoms of fever and cough whereas it was negatively correlated with mid‐upper arm circumference (MUAC), weight‐for‐height z score (WHZ), edema, and dermatosis.Conclusions:Children with complicated SAM seem to have impaired gut function characterized by reduced enterocyte mass, intestinal inflammation, and increased bacterial translocation.
A test of psychological and electrodermal changes immediately after the delivery of 3 analgesic treatment messages
Authors: Geers Andrew L. , Fowler Stephanie L. , Helfer Suzanne G. , Murray Ashley B. 
Published: June 2019

Abstract

Introduction:
Placebo analgesia often results when a pain reduction treatment message is delivered to a patient or research participant. Little information exists regarding the psychological changes that are immediately triggered by the delivery of a treatment message.

Objectives:
This experiment tested the impact of 3 different analgesic treatment messages on the expectations, feelings, and electrodermal activity of participants anticipating a pain stimulus.

Methods:
In laboratory sessions, healthy participants (N = 138) were randomly assigned to 1 of 4 conditions in a between-subject design. The design included a no treatment message control condition and 3 treatment message conditions: a standard analgesic message, an analgesic treatment with side-effect message, and a double-blind analgesic message. After the treatment message manipulation, measures were taken of: treatment efficacy expectations, pain experience expectations, pretask anxiety, positive affect, negative affect, and electrodermal activity.

Results:
Overall, the dependent measures showed relatively few correlations. Furthermore, across all 3 message conditions, treatment-specific expectations were greatly increased compared with the control condition. Finally, participants in the double-blind message condition displayed elevated negative affect.

Conclusion:
All 3 analgesic treatment messages produced a stronger immediate influence on treatment efficacy expectations than on the other dependent measures. Treatment messages can alter negative affect along with expectancies. The low correlations found between dependent measures suggest that different patterns of psychological responses may emerge from analgesic treatment messages depending on contextual factors.
Shared HCV Transmission Networks Among HIV-1–Positive and HIV-1–Negative Men Having Sex With Men by Ultradeep Sequencing
Authors: Nguyen Thuy , Delaugerre Constance , Valantin Marc-Antoine , Amiel Corinne , Netzer Emmanuelle , L'yavanc Thomas , Ohayon Michel , Valin Nadia , Day Nesrine , Kreplak Georges , Pialoux Gilles , Calvez Vincent , Molina Jean-Michel , Marcelin Anne-Geneviève , Todesco Eve 
Published: June 2019

Objective:
Several studies reported hepatitis C virus (HCV) transmission networks among men having sex with men (MSM) in Europe and the spread of HCV strains from HIV–HCV coinfected toward HCV monoinfected MSM. We aimed to investigate HCV transmission dynamics among HIV-positive and HIV-negative MSM by ultradeep sequencing (UDS).

Design and Methods:
NS5B fragment (388 bp) was sequenced from virus of 50 HIV-positive and 18 HIV-negative patients diagnosed with recent HCV infection. UDS data were analyzed by Geneious (version 10.3.2). Phylogenetic trees were constructed by FastTree (version 2.1) and submitted to ClusterPicker (version 1.2.3) for transmission chain detection at different thresholds of maximum genetic distance (MGD) (3% for Sanger, 3% and 4.5% for UDS).

Results:
Ten, 17, and 18 HCV transmission chains were identified by Sanger at 3%, UDS at 3% and at 4.5% of MGD, respectively. Of 68 subjects enrolled, 38 (55.9%), 38 (55.9%), and 43 (65.3%) individuals were involved in transmission networks found by Sanger at 3%, UDS at 3%, and at 4.5% of MGD, respectively. Mixed transmission chains including HIV-positive and HIV-negative subjects were detected for 8/10 chains by Sanger at 3%, for 9/17 by UDS at 3%, and for 10/18 by UDS at 4.5% of MGD. Overall, the number of HIV-negative individuals clustering with HIV-positive ones was 9/18 by Sanger, 9/18 by UDS at 3%, and 10/18 by UDS at 4.5% of MGD.

Conclusions:
HIV-positive and HIV-negative MSM shared HCV transmission networks, which emphasizes the need for HCV surveillance and prevention measures in these communities regardless of the HIV status.
Primary familial brain calcifications: genetic and clinical update
Authors: Westenberger Ana , Balck Alexander , Klein Christine 
Published: June 2019

Purpose of review
In the last 7 years, changes in five genes [SLC20A2, PDGFRB, PDGFB, XPR1, and MYORG] have been implicated in the pathogenesis of primary familial brain calcification (PFBC), allowing for genetic delineation of this phenotypically complex neurodegenerative disorder. This review explores how the ensuing plethora of reported PFBC patients and their disease-causing variants improved our understanding of disease, pathogenesis, clinical manifestation, and penetrance.

Recent findings
In PFBC patients, pathogenic changes have been most frequently described in SLC20A2, accounting for approximately the same number of patients as the variants in the other four PFBC genes combined. There is no appreciable relationship between any combination of the following three variables: the type of disease-causing change, the pattern or extent of calcifications, and the presence or nature of clinical manifestation in PFBC patients. Nevertheless, elucidation of underlying genetic factors provided important recent insights into the pathogenic mechanisms of PFBC, which collectively point toward a compromised neurovascular unit.

Summary
The ongoing clinical and molecular research increases our understanding of PFBC facilitating diagnosis and identifying potential therapeutic targets for this multifaceted and likely underdiagnosed condition.
A nation-wide initiative for brain imaging and clinical phenotype data federation in Swiss university memory centres
Authors: Draganski Bogdan , Kherif Ferath , Damian Daniel , Demonet Jean-Francois 
Published: June 2019

Purpose of review
The goal of our nation-wide initiative is to provide clinicians intuitive and robust tools for accurate diagnosis, therapy monitoring and prognosis of cognitive decline that is based on large-scale multidomain data.

Recent findings
We describe a federation framework that allows for statistical analysis of aggregated brain imaging and clinical phenotyping data across memory clinics in Switzerland. The adaptation and deployment of readily available data capturing and federation modules is paralleled by developments in ontology, quality and regulatory control of brain imaging data. Our initiative incentivizes data sharing through the common resource in a way that provides individual researcher with access to large-scale data that surpasses the data acquisition capacity of a single centre. Clinicians benefit from fine-grained epidemiological characterization of own data compared with the rest additional to intuitive tools allowing for computer-based diagnosis of dementia. Finally, our concept aims at closing the loop between group-level results based on aggregate data and individual diagnosis by providing disease models, that is, classifiers for neurocognitive disorders that will enable the computer-based diagnosis of individual patients.

Summary
The obtained results will inform recommendations on best clinical practice in all relevant fields focusing on standardization and interoperability of acquired data, privacy protection framework and ethical consideration in the context of evolutive pathology.
Disentangled behavioral representations
Authors: Dezfouli Amir , Ashtiani Hassan , Ghattas Omar , Nock Richard , Dayan Peter , Ong Cheng Soon 
Published: June 2019

AbstractIndividual characteristics in human decision-making are often quantified by fitting a parametric cognitive model to subjects’ behavior and then studying differences between them in the associated parameter space. However, these models often fit behavior more poorly than recurrent neural networks (RNNs), which are more flexible and make fewer assumptions about the underlying decision-making processes. Unfortunately, the parameter and latent activity spaces of RNNs are generally high-dimensional and uninterpretable, making it hard to use them to study individual differences. Here, we show how to benefit from the flexibility of RNNs while representing individual differences in a low-dimensional and interpretable space. To achieve this, we propose a novel end-to-end learning framework in which an encoder is trained to map the behavior of subjects into a low-dimensional latent space. These low-dimensional representations are used to generate the parameters of individual RNNs corresponding to the decision-making process of each subject. We introduce terms into the loss function that ensure that the latent dimensions are informative and disentangled, i.e., encouraged to have distinct effects on behavior. This allows them to align with separate facets of individual differences. We illustrate the performance of our framework on synthetic data as well as a dataset including the behavior of patients with psychiatric disorders.
Highly reliable, targeted photothermal cancer therapy combined with thermal dosimetry using indocyanine green lactosome
Authors: Nomura Shinsuke , Morimoto Yuji , Tsujimoto Hironori , Harada Manabu , Saitoh Daizoh , Hara Isao , Ozeki Eiichi , Satoh Ayano , Takayama Eiji , Hase Kazuo , Kishi Yoji , Ueno Hideki 
Published: June 2019

AbstractIndocyanine green (ICG) is a near-infrared light-absorbing substance. Thus, when a tumor in which ICG has accumulated is irradiated with a near-infrared (NIR) laser, only the tumor can be heated by a photothermal reaction. We developed ICG lactosome, a novel drug delivery system (DDS) composed of polymeric micelles and ICG that shows selective accumulation in tumor based on an enhanced permeability and retention (EPR) effect. We showed that ICG lactosome accumulated in a tumor by using an intradermal tumor mouse model of a murine colon cancer cell line (Colon26) transfected with Nano lantern luminescent protein (NLC26). Two days after the administration of ICG lactosome, the tumor was irradiated with an 808-nm diode-laser while monitoring tumor temperature. The results showed that the treated tumors were cured when the peak of tumor temperature during NIR irradiation reached 43°C or higher. To verify these results, photothermal therapy (PTT) using ICG lactosome was carried out using a newly developed system that can control the temperature at the NIR irradiation site at a constant level. All of the tumors that had been kept at 43°C during irradiation were cured, while 2 of 5 tumors that had been kept at 42°C were not cured, and none of tumors that had been kept at a temperature below 41°C were cured. ICG lactosome-assisted PTT combined with thermal dosimetry is a highly reliable method for cancer treatment and may afford further clinical opportunities for PTT.
Choosing what we like vs liking what we choose: How choice-induced preference change might actually be instrumental to decision-making
Authors: Lee Douglas , Daunizeau Jean 
Published: June 2019

ABSTRACTFor more than 60 years, it has been known that people report higher (lower) subjective values for items after having selected (rejected) them during a choice task. This phenomenon is coined “choice-induced preference change” or CIPC, and its established interpretation is that of “cognitive dissonance” theory. In brief, if people feel uneasy about their choice, they later convince themselves, albeit not always consciously, that the chosen (rejected) item was actually better (worse) than they had originally estimated. While this might make sense from a pragmatic psychological standpoint, it is challenging from a theoretical evolutionary perspective. This is because such a cognitive mechanism might yield irrational biases, whose adaptive fitness would be unclear. In this work, we assume that CIPC is mostly driven by the refinement of option value representations that occurs during (and not after) difficult choices. This makes CIPC the epiphenomenal outcome of a cognitive process that is instrumental to the decision. Critically, our hypothesis implies novel predictions about how observed CIPC should relate to two specific meta-cognitive processes, namely: choice confidence and subjective certainty regarding pre-choice value judgments. We test these predictions in a behavioral experiment where participants rate the subjective value of food items both before and after choosing between equally valued items; we augment this traditional design with reports of choice confidence and subjective certainty about value judgments. The results confirm our predictions and provide evidence against the standard post-choice cognitive dissonance reduction explanation. We then discuss the relevance of our work in the context of the existing debate regarding the putative cognitive mechanisms underlying cognitive dissonance reduction.
An ancestral apical brain region contributes to the central complex under the control offoxQ2in the beetleTribolium castaneum
Authors: He Bicheng , Buescher Marita , Farnworth Max Stephen , Strobl Frederic , Stelzer Ernst , Koniszewski Nikolaus Dieter Bernhard , Mühlen Dominik , Bucher Gregor 
Published: June 2019

AbstractThe genetic control of anterior brain development is highly conserved throughout animals. For instance, a conserved anterior gene regulatory network specifies the ancestral neuroendocrine center of animals and the apical organ of marine organisms. However, its contribution to the brain in non-marine animals has remained elusive. Here, we study the function of theTc-foxQ2forkhead transcription factor, a key regulator of the anterior gene regulatory network of insects. We characterized four distinct types ofTc-foxQ2positive neural progenitor cells based on differential co-expression withTc-six3/optix, Tc-six4, Tc-chx/vsx, Tc-nkx2.1/scro, Tc-ey, Tc-rxandTc-fez1. An enhancer trap line built by genome editing markedTc-foxQ2positive neurons, which projected through the primary brain commissure and later through a subset of commissural fascicles. Eventually, they contributed to the central complex. Strikingly, inTc-foxQ2RNAi knock-down embryos the primary brain commissure did not split and subsequent development of midline brain structures stalled. Our work establishesfoxQ2as a key regulator of brain midline structures, which distinguish the protocerebrum from segmental ganglia. Unexpectedly, our data suggest that the central complex evolved by integrating neural cells from an ancestral anterior neuroendocrine center.Summary statementAn ancestral neuroendocrine center contributes to the evolution of the central complex.foxQ2is a gene required for the development of midline structures of the insect brain, which distinguish protocerebrum from segmental ganglia.
Evidence for Membrane Complex Assembly in Nanoelectrospray Generated Lipid Bilayers
Authors: Wilm Matthias 
Published: June 2019

1.AbstractNanoelectrospray can be used to generate a layered structure consisting of bipolar lipids, detergent-solubilized membrane proteins, and glycerol that self-assembles upon detergent extraction into one extended layer of a protein containing membrane. This manuscript presents the first evidence that this method might allow membrane protein complexes to assemble in this process.
ESCRT machinery mediates selective microautophagy of endoplasmic reticulum
Authors: Schäfer Jasmin A. , Schessner Julia P. , Bircham Peter W. , Tsuji Takuma , Funaya Charlotta , Schaeff Katharina , Ruffini Giulia , Papagiannidis Dimitrios , Knop Michael , Fujimoto Toyoshi , Schuck Sebastian 
Published: June 2019

ABSTRACTER-phagy, the selective autophagy of endoplasmic reticulum (ER), safeguards organelle homeostasis by eliminating misfolded proteins and regulating ER size. ER-phagy can occur by macroautophagic and microautophagic mechanisms. While dedicated machinery for macro-ER-phagy has been discovered, the molecules and mechanisms mediating micro-ER-phagy remain unknown. Here, we first show that micro-ER-phagy in yeast involves the conversion of stacked cisternal ER into multilamellar ER whorls during microautophagic uptake into lysosomes. Second, we identify the conserved Nem1-Spo7 phosphatase complex and ESCRT proteins as key components for micro-ER-phagy. Third, we demonstrate that macro- and micro-ER-phagy are parallel pathways with distinct molecular requirements. Finally, we provide evidence that ESCRT proteins directly function in scission of the lysosomal membrane to complete the microautophagic uptake of ER. These findings establish a framework for a mechanistic understanding of micro-ER-phagy and, thus, a comprehensive appreciation of the role of autophagy in ER homeostasis.
Combinatorial proteomics and transcriptomics identify AMPK in the control of the axonal regeneration programme of DRG sensory neurons after spinal injury
Authors: Kong Guiping , Zhou Luming , Serger Elisabeth , Palmisano Ilaria , De Virgiliis Francesco , Hutson Thomas H , Mclachlan Eilidh , Freiwald Anja , La Montanara Paolo , Shkura Kirill , Puttagunta Radhika , Di Giovanni Simone 
Published: June 2019

SUMMARYRegeneration after injury occurs in axons that lie in the peripheral nervous system but it fails in the central nervous system limiting functional recovery. Despite recent progress, the signalling response to injury of peripheral versus central projecting axons that might underpin this differential regenerative ability is currently largely uncharacterized. To fill this knowledge gap, here we combined axoplasmic proteomics from peripheral sciatic or central projecting dorsal root axons from sciatic DRG neurons. Proteomics was combined with cell body RNAseq to compare axonal and soma responses between a spinal regeneration-incompetent versus sciatic regeneration-competent nerve injury. This allowed the identification of injury-dependent signalling pathways uniquely represented in peripheral versus central projecting sciatic DRG axons. RNAseq and proteomics analysis suggested AMPK as a putative regulator of axonal regenerative signalling pathways. AMPK immunoprecipitation followed by mass spectrometry from DRG suggested that the 26S proteasome and its regulatory subunit PSMC5 preferentially interact with AMPKα for proteasomal degradation following sciatic axotomy. Mechanistically, we found that the proteasome and CaMKIIα-dependent proteasomal subunit PSMC5 regulates AMPKα1 protein expression. Finally, conditional deletion of AMPKα1 promoted multiple regenerative signalling pathways and robust axonal growth across the injured spinal cord, suggesting inhibition of AMPK as a novel regenerative target following spinal injury.HIGHLIGHTSAxoplasmic proteomics from sciatic or centrally projecting branches of sciatic DRG identifies unique protein enrichment and signalling pathways, including prior and subsequent to a spinal regeneration-incompetent versus sciatic regeneration-competent axonal injuryCombined axoplasmic DRG proteomics and cell body RNAseq analysis suggest AMPK as a central regulator controlling axonal regenerationThe 26S proteasome and the 19S regulatory subunit PSMC5 interact with AMPKα following sciatic axotomy. PSMC5 regulates AMPKα1 protein levelsAMPKα1 conditional deletion enhances robust axonal growth following SCI
FALCONET: an R package to accelerate automatic visualisation of genome scale metabolic models
Authors: Lu Hongzhong , Zhu Zhengming , Kerkhoven Eduard J , Nielsen Jens 
Published: June 2019

AbstractSummaryFALCONET (FAst visuaLisation of COmputational NETworks) enables the automatic for-mation and visualisation of metabolic maps from genome-scale models with R and CellDesigner, readily facilitating the visualisation of multi-layers omics datasets in the context of metabolic networks.MotivationUntil now, numerous GEMs have been reconstructed and used as scaffolds to conduct integrative omics analysis and in silico strain design. Due to the large network size of GEMs, it is challenging to produce and visualize these networks as metabolic maps for further in-depth analyses.ResultsHere, we presented the R package - FALCONET, which facilitates drawing and visualizing metabolic maps in an automatic manner. This package will benefit the research community by allowing a wider use of GEMs in systems biology.Availability and implementationFALCONET is available on https://github.com/SysBioChalmers/FALCONET and released under the MIT License.Contactnielsenj@chalmers.seSupplementary informationSupplementary data are available online.