bluuebunny/crossref_metadata_2025_split huggingface dataset:
On Avoiding Deep Dementia
Authors: Cantor Norman L. 
Published: August 2018

AbstractSome people will confront Alzheimer's with a measure of resignation, a determination to struggle against the progressive debilitation and to extract whatever comforts and benefits they can from their remaining existence. They are entitled to pursue that resolute path. For other people, like myself, protracted maintenance during progressive cognitive dysfunction and helplessness is an intolerably degrading prospect. The critical question for those of us seeking to avoid protracted dementia is how best to accomplish that objective.One strategy is to engineer one's own death while still mentally competent to do so (even in the stage of mild dementia). If I were to use a preemptive strategy in the face of a dementia diagnosis, I would probably choose to stop eating and drinking, a process known as voluntarily stopping eating and drinking. An alternative tactic for avoiding prolonged dementia would be to allow oneself to decline into moderate dementia—thus losing capacity to perform self‐deliverance or even to make serious medical decisions—but before getting to that point to provide advance instructions rejecting prospective life‐sustaining medical interventions. These advance instructions would authorize palliative but not curative measures. My current personal instructions define the point of intolerable cognitive decline triggering medical nonintervention as “mental deterioration to a point when I can no longer read and understand written material such as a newspaper or financial records such as a checkbook.” These instructions dictate allowing my demise at a point of moderate dementia when I may not be perceptibly suffering, when I may still be getting some rudimentary satisfaction from my debilitated life, and when I no longer recall the preoccupation with personally intolerable indignity that motivated my instructions. Can I expect that my advance instructions will be implemented in those circumstances? Is it lawful, and is it moral for a surrogate decision‐maker and associated caregivers to allow an uncomprehending, ostensibly content but demented individual to die? My analysis herein contends that it is not only lawful and moral but also legally required to implement clear, considered advance instructions even at a stage of moderate dementia.
An Open Letter to Norman Cantor Regarding Dementia and Physician‐Assisted Suicide
Authors: Sulmasy Daniel P. 
Published: August 2018

AbstractDear Norm,Thank you for sharing such a personal and heartfelt essay. I have been asked by the editors to comment. Reading it inspires me to do so in a similarly heartfelt way. Although I don't know you well, I thought I'd write to you as if you were my patient.I share your sense that Alzheimer disease is a terrible scourge. I've seen much of this disease over a lifetime of practice, and I deeply understand its ravages and the debility and suffering it causes. But what you propose is not a good solution for the problems that Alzheimer disease poses for patients, families, and society. It will ultimately do far more harm than good. Please let me try to explain.
Modulation of network‐to‐network connectivity via spike‐timing‐dependent noninvasive brain stimulation
Authors: Santarnecchi Emiliano , Momi Davide , Sprugnoli Giulia , Neri Francesco , Pascual‐Leone Alvaro , Rossi Alessandro , Rossi Simone 
Published: August 2018

AbstractHuman cognitive abilities and behavior are linked to functional coupling of many brain regions organized in distinct networks. Gaining insights on the role those networks’ dynamics play in cognition and pathology requires their selective, reliable, and reversible manipulation. Here we document the possibility to manipulate the interplay between two brain networks in a controlled manner, by means of a Transcranial Magnetic Stimulation (TMS) protocol inducing spike timing dependent plasticity (STDP). Pairs of TMS pulses at specific inter‐stimulus intervals, repeatedly delivered over two negatively correlated nodes of the default mode network (DMN) and the task‐positive network (TPN) defined on the basis of individual functional magnetic resonance imaging (fMRI) data, induced a modulation of network‐to‐network connectivity, even reversing correlation from negative to slightly positive in 30% of cases. Results also suggest a baseline‐dependent effect, with a greater connectivity modulation observed in participants with weaker between‐networks connectivity strength right before TMS. Finally, modulation of task‐evoked fMRI activity patterns during a sustained attention task was also observed after stimulation, with a faster or slower switch between rest and task blocks according to the timing of TMS pulses. The present findings promote paired associative TMS as a promising technique for controlled manipulation of fMRI connectivity dynamics in humans, as well as the causal investigation of brain‐behavior relations.
Structural and functional cerebral bases of diminished inhibitory control during healthy aging
Authors: Hu Sien , Ide Jaime S. , Chao Herta H. , Castagna Brittney , Fischer Kimberly A. , Zhang Sheng , Li Chiang‐shan R. 
Published: August 2018

AbstractInhibitory control or the ability to refrain from incorrect responses is a critical executive function known to diminish during aging. Imaging studies have elucidated cerebral changes that may underlie the age‐related deficits. However, it remains unclear whether the structural and functional changes occur in the same brain regions and whether reduced gray matter volumes (GMV) mediate decreased activation during inhibition. Here, in a sample of 149 participants, we addressed the issues using structural and functional magnetic resonance imaging. Individual's response inhibition was evaluated by the stop signal reaction time (SSRT) in a stop signal task. The results showed that age was associated with prolonged SSRT across participants. Many cortical and subcortical regions demonstrated age‐related reduction in GMV and activation to response inhibition. Additionally, age‐related diminution in inhibitory control, as indexed by the SSRT, was associated with both shared and distinct morphometric and functional changes. Voxel‐based morphometry demonstrated age‐related reduction in GMV in the right dorsolateral prefrontal cortex and caudate head as well as bilateral insula, in association with prolonged SSRT. In a contrast of stop success versus go success trials, age was associated with lower activation in the medial and inferior frontal cortex and inferior parietal cortex. Further, reduction in GMV mediated age‐related differences in activations only of the medial prefrontal cortex, providing limited evidence for structure function association. Thus, the decline in inhibitory control, as evidenced in the stop signal task, manifest with both shared and distinct structural and functional processes during aging.
Sources of health financing and health outcomes: A panel data analysis
Authors: Fujii Tomoki 
Published: August 2018

AbstractWe study the differential impacts of public and private sources of health spending on health outcomes using a triple difference approach. We find that private health spending has on average a higher health‐promoting effect than public health spending. This result is robust with respect to the choice of outcome measure and covariates in the regression and driven primarily by the countries with ineffective governments. Once we restrict our sample to countries with effective governments, private health spending is found to be no better than public health spending in improving the health outcome.
The effects of topography and forest management on water storage in catchments in south‐central Chile
Authors: Barrientos Guillermo , Iroumé Andrés 
Published: August 2018

AbstractOur work analyses the intra‐annual variability of the volume of water stored in 15 forested headwater catchments from south‐central Chile, aiming at understanding how forest management, hydrology, and climate influence the dynamic components of catchment storage. Thus, we address the following questions: (a) How does the annual water storage vary in catchments located in diverse hydroclimatic conditions and subject to variable forest management? (b) Which natural (i.e., hydrologic regime and physiographic setting) and anthropogenic factors explain the variance in water storage? Results show that the annual catchment storage increases at the beginning of each hydrological year in direct response to increases in rainfall. The maximum water storage ranges from 666 to 1,272 mm in these catchments. The catchments with Pinus or Eucalyptus spp. cover store less water than the catchments with mixed forest species cover. Forest cover (biomass volume, plantation density, and percentage of plantation and age) has the primary control on dynamic storage in all catchments. These results indicate that forest management may alter the catchment water storage.
Synthesis and Applications of Endohedrally Functionalized Metal‐Ligand Cage Complexes
Authors: Bogie Paul M. , Miller Tabitha F. , Hooley Richard J. 
Published: August 2018

AbstractSelf‐assembled cages have garnered wide‐spread interest as supramolecular hosts. Their abilities may be augmented through the installation of functional groups on the interior of the cage. This article highlights recent advances in the applications of endohedral functionalization in control of overall self‐assembly, molecular recognition and reactivity, with an emphasis on installing functionalization that enables biomimetic catalysis.
Identification of synthetic lethality based on a functional network by using machine learning algorithms
Authors: Li JiaRui , Lu Lin , Zhang Yu‐Hang , Liu Min , Chen Lei , Huang Tao , Cai Yu‐Dong 
Published: August 2018

AbstractSynthetic lethality is the synthesis of mutations leading to cell death. Tumor‐specific synthetic lethality has been targeted in research to improve cancer therapy. With the advances of techniques in molecular biology, such as RNAi and CRISPR/Cas9 gene editing, efforts have been made to systematically identify synthetic lethal interactions, especially for frequently mutated genes in cancers. However, elucidating the mechanism of synthetic lethality remains a challenge because of the complexity of its influencing conditions. In this study, we proposed a new computational method to identify critical functional features that can accurately predict synthetic lethal interactions. This method incorporates several machine learning algorithms and encodes protein‐coding genes by an enrichment system derived from gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways to represent their functional features. We built a random forest‐based prediction engine by using 2120 selected features and obtained a Matthews correlation coefficient of 0.532. We examined the top 15 features and found that most of them have potential roles in synthetic lethality according to previous studies. These results demonstrate the ability of our proposed method to predict synthetic lethal interactions and provide a basis for further characterization of these particular genetic combinations.
Ulinastatin attenuates liver injury and inflammation in a cecal ligation and puncture induced sepsis mouse model
Authors: Song Yukang , Miao Shixing , Li Yexuzi , Fu Hui 
Published: August 2018

AbstractSepsis is a syndrome of life‐threatening multiorgan dysfunction caused by host response dysregulation to infection. Ulinastatin (UTI), a serine protease inhibitor, possesses anti‐inflammatory properties and has been suggested to modulate lipopolysaccharide‐induced sepsis. However, little is known about the mechanism underlying its effects on sepsis. In the current study, we investigated the protective effect of UTI on liver injury in a cecal ligation and puncture (CLP)‐induced sepsis of C57BL/6 mouse model and explored the possible mechanisms. Mice underwent CLP as sepsis models and were randomized into five groups including the sham group, UTI group, CLP group, UTI‐L group, and UTI‐H group. UTI was intraperitoneally administered at doses of UTI 1500 U/100 g (UTI‐L group) or 3000 U/100 g (UTI‐H group), before CLP. The mice were killed, and immunohistochemical changes, cytokine levels, and antioxidant enzyme activities were detected. Our results showed that UTI ameliorated CLP‐mediated increases in serum aspartate aminotransferase and alanine aminotransferase activities, histological activity index, degenerative region ratio, and infiltrated inflammatory cell numbers. Moreover, UTI also decreased nitrotyrosine and 4‐hydroxynonenal, activated caspase‐3, and activated poly (ADP‐ribose) polymerase (PARP) levels and inhibited the mitogen‐activated protein kinase pathway activation in liver tissues. Our results indicated that UTI could inhibit CLP‐induced liver injury by suppressing inflammation and oxidation. Our results indicated that UTI may serve as a potential therapeutic agent for sepsis.
Transcriptome mining of non‐BRCA1/A2 and BRCA1/A2 familial breast cancer
Authors: Akbari Vahid , Kallhor Marzieh , Akbari Mohammad Taghi 
Published: August 2018

AbstractAbout 10% of all breast cancer cases are the familial type. Mutations in two highly penetrance breast cancer susceptibility genes, BRCA1 and BRCA2, can only explain 20% to 25% of genetic susceptibility to breast cancer, and most familial breast cancer cases have intact BRCA1 and BRCA2 genes that refer to non‐BRCA1/A2 or BRCAX familial breast cancer. Despite extensive studies, more than 50% of genetic susceptibility to breast cancer remained to be disclosed. Finding the differences between these two types of breast cancer (non‐BRCA1/A2 and BRCA1/A2) at genomic, transcriptomic, and proteomic levels can help us to elucidate fundamental molecular processes and develope more promising therapeutic targets. Here, we used expression data of 391 patients with familial breast cancer including 195 non‐BRCA1/A2 and 196 BRCA1 and/or BRCA2 cases from four independent studies by means of meta‐analysis to find differences in gene expression signature between these two types of familial breast cancer. As well as, we applied comprehensive network analysis to find crucial protein complexes and regulators for each condition. Our results revealed significant overexpression of cell cycle processes in BRCA1/A2 patients and significant overexpression of estrogen axis in non‐BRCA1/A2 patients. Moreover, we found FOXM1 as the central regulator of cell cycle processes and GATA3, FOXA1, and ESR1 as the main regulators of estrogen axis.
Molecular characterization of lung adenocarcinoma: A potential four–long noncoding RNA prognostic signature
Authors: Sui Jing , Yang Sheng , Liu Tong , Wu Wenjuan , Xu Siyi , Yin Lihong , Pu Yuepu , Zhang Xiaomei , Zhang Yan , Shen Bo , Liang Geyu 
Published: August 2018

AbstractBackgroundLung adenocarcinoma (LUAD), mainly originated in lung glandular cells, is the most frequent pathological type of lung cancer and the 5‐year survival rate of LUAD patients is still very low. Therefore, we aim to identify a long noncoding RNA (lncRNA)–related signature as the sensitive and novel prognostic biomarkers.MethodsThe associations between survival outcome and the intersection of lncRNAs were obtained from The Cancer Genome Atlas (TCGA) database. By the univariate and multivariate Cox analyses, key lncRNAs were identified to construct the prognostic model. The model was estimated by survival analysis and receiver operating characteristic curve, and verified by the Kaplan‐Meier (K‐M) plotter and quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). Functional enrichment analysis was also performed.ResultsA four‐lncRNA signature (CEBPA‐AS1, GVINP1, MIR31HG, and RAET1K) was developed after Cox analysis. The power of the four‐lncRNA prognostic signature was effective in the TCGA database. The results from by the K‐M plotter and qRT‐PCR validation were consistent with our TCGA bioinformatics results. Furthermore, Gene Ontology and pathway analysis revealed the tumorigenic and prognostic function of the four lncRNAs.ConclusionsBy mining the TCGA data, we built a four‐lncRNA signature, which could effectively predict prognosis of LUAD. In the future, an independent cohort is needed to validate our findings.ImpactThe four‐lncRNA signature could become potential prognostic indicator of LUAD in the future.
Retracted: Deletion of long noncoding RNA EFNA3 aggravates hypoxia‐induced injury in PC‐12 cells by upregulation of miR‐101a
Authors: Gong Weijun , Qie Shuyan , Huang Peiling , Xi Jianing 
Published: August 2018

AbstractLong noncoding RNAs (lncRNAs) have been reported to be involved in several neurological pathogenesis conditions including cerebral ischemia. In the current study, the functions of lncRNA EFNA3 on hypoxia‐injured rat adrenal pheochromocytoma (PC‐12) cells and the underlying molecular mechanism were studied. The expression of lncRNA EFNA3 was silenced by short hairpin RNA transfection, after which the cells were subjected with hypoxia. Cell viability, migration, invasion, and apoptosis were, respectively, determined by trypan blue staining, Transwell assay, annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI) double‐staining, and Western blot analysis. The cross regulation between lncRNA EFNA3 and miR‐101a, as well as between miR‐101a and Rho associated coiled‐coil containing protein kinase 2 (ROCK2) were detected by performing quantitative real‐time polymerase chain reaction, RNA pull‐down, RNA immunoprecipitation, luciferase activity assay, and Western blot analysis. Studies showed that lncRNA EFNA3 was highly expressed in response to hypoxia. Deletion of lncRNA EFNA3 significantly aggravated hypoxia‐induced injury in PC‐12 cells, as the impairment of cell viability, migration, and invasion, and the inducement of apoptosis. LncRNA EFNA3 worked as a sponging molecule for miR‐101a and miR‐101a suppression‐protected PC‐12 cells against hypoxia‐induced injury even when lncRNA EFNA3 was silenced. ROCK2 was a target gene of miR‐101a. ROCK2 overexpression exhibited neuroprotective activities. Besides, ROCK2 overexpression activated Wnt/β‐catenin pathway whereas it deactivated JAK/STAT pathway upon hypoxia. Our study suggests that deletion of lncRNA EFNA3 aggravates hypoxia‐induced injury in PC‐12 cells by upregulating miR‐101a, which further targets ROCK2.
Ultrasonography and autopsy correlation of fetal hypoplastic left heart syndrome
Authors: Kumar Manisha , Priyam  
Published: August 2018

AbstractHypoplastic left heart syndrome (HLHS) represents a spectrum of abnormalities which marks the underdevelopment of left side cardiac structures. We present the ultrasound and autopsy correlation of two cases with HLHS with core pathology as isolated mitral atresia in one and aortic atresia in another. In both the cases after diagnostic confirmation on ultrasound (US), the couple opted for termination of pregnancy and consented for autopsy. The correlation of US and autopsy images of HLHS, facilitated our understanding of pathology behind the image obtained on US. The autopsy not only confirmed the antenatal diagnosis, but also added new findings.
Autoimmunity and immune system dysregulation in schizophrenia: IgGs from sera of patients hydrolyze myelin basic protein
Authors: Parshukova Daria , Smirnova Liudmila P. , Ermakov Evgeny A. , Bokhan Nikolay A. , Semke Arkadiy V. , Ivanova Svetlana A. , Buneva Valentina N. , Nevinsky Georgy A. 
Published: August 2018

AbstractSeveral different theories of schizophrenia (SCZ) were discussed; the causes of this disease are not yet clear. Using ELISA, it was shown that titers of autoantibodies against myelin basic protein (MBP) in SCZ patients are ~1.8‐fold higher than in healthy individuals but 5.0‐fold lower than in patients with multiple sclerosis. Several rigid criteria were checked to show that the MBP‐hydrolyzing activity is an intrinsic property of SCZ IgGs. Approximately 82% electrophoretically homogeneous SCZ IgGs purified using several affinity sorbents including Sepharose with immobilized MBP hydrolyze specifically only MBP but not many other tested proteins. The average relative activity of IgGs from patients with negative symptoms was 2.5‐fold higher than that of patients with positive symptoms of SCZ, and it increases with the duration of this pathology. It was shown that abzymes are the earliest statistically significant markers of many autoimmune pathologies. Our findings surmise that the immune systems of individual SCZ patients can generate a variety of anti‐MBP abzymes with different catalytic properties, which can attack MBP of the myelin‐proteolipid shell of axons. Therefore, autoimmune processes together with other mechanisms can play an important role in SCZ pathogenesis. MBP‐hydrolyzing antibodies were previously detected in the blood of 80% to 90% of patients with systemic lupus erythematosus (SLE) and multiple sclerosis (MS). In addition, some similar neuropsychiatric indicators of disease common to SLE, MS, and SCZ were described in the literature. Thus, the destruction of the myelin sheath and the production of MBP‐hydrolyzing antibodies can be a common phenomenon for some different diseases.
Limitation of the bandpass filter in preventing oversensing of pectoral myopotentials over the long‐term follow‐up
Authors: Hori Yuichi , Nakahara Shiro , Nishiyama Naoki , Fukuda Reiko , Toratani Noritaka , Sakai Yoshihiko , Taguchi Isao 
Published: August 2018

AbstractA 60‐year‐old male experienced an inappropriate shock from an implantable cardioverter‐defibrillator (ICD) because of oversensing of pectoral myopotentials. Battery depletion was also observed, and a generator change was performed. A single‐chamber ICD (VENTAK PRIZM II 1860) was changed to a new ICD (INCEPTA VR F161). The myopotentials were clearly eliminated by the difference in the band pass filter (PRIZM; 21‐171 Hz, INCEPTA; 20‐85 Hz), but unfortunately, new noise was documented 4 years later. The utility of the bandpass filter for preventing oversensing of myopotentials was observed, but the limitation of its use for long‐term follow‐up was also indicated.
Seedball‐induced changes of root growth and physico‐chemical properties—a case study with pearl millet
Authors: Nwankwo Charles I. , Blaser Sebastian R. G. A. , Vetterlein Doris , Neumann Günter , Herrmann Ludger 
Published: August 2018

AbstractSeedball is a cheap “seed‐pelleting‐technique” that combines local materials, seeds and optionally additives such as mineral fertilizer to enhance pearl millet (Pennisetum glaucum (L.) R. Brown) early growth under poor soil conditions. The major objective here was to study the mechanisms behind positive seedball effects. Chemical effects in the rhizosphere and early root development of seedball‐derived pearl millet seedlings were monitored using micro‐suction‐cups to extract soil solutions and X‐ray tomography to visualize early root growth. Pearl millet (single seedling) was grown in soil columns in a sandy soil substrate. Root and shoot biomass were sampled. X‐ray tomography imaging revealed intense development of fine roots within the nutrient‐amended seedball. Seedball and seedball+NPK treatments, respectively, were 65% and 165% higher in shoot fresh weight, and 108% and 227% higher in shoot dry matter than the control treatment. Seedball+NPK seedlings showed promoted root growth in the upper compartment and 105% and 30% increments in root fresh and dry weights. Soil solution concentrations indicate that fine root growth ass stimulated by release of nutrients from the seedballs to their direct proximity. Under real field conditions, the higher root length density and finer roots could improve seedlings survival under early drought conditions due to better ability to extract water and nutrients from a greater soil volume.