bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recent History of Serious Fall Injuries and Posttransplant Outcomes Among US Kidney Transplant Recipients
Authors: Lynch Raymond J. , Patzer Rachel E. , Pastan Stephen O. , Bowling C. Barrett , Plantinga Laura C. 
Published: September 2018

Background.
Serious fall injuries are associated with poor outcomes among dialysis patients, but whether these associations hold in patients with a history of serious fall injury before kidney transplantation is unknown.

Methods.
In national administrative data, 22 474 US adults receiving a first kidney transplant in 2011–2014 with at least 1 year of follow-up before transplant were identified. Serious fall injuries in the year before transplant were identified using diagnostic codes for falls and simultaneous fractures, dislocations, or head trauma in inpatient or outpatient claims. We used multivariable Cox proportional hazards models to estimate associations of incident posttransplant outcomes with serious fall injury in the year before transplant.

Results.
A total of 620 (2.8%) recipients had serious fall injuries before transplant and were more likely to be white, female, and have more comorbid conditions than those without a fall injury. Although posttransplant recipient survival did not differ by recent serious fall injuries (hazard ratio [HR], 1.03; 95% confidence interval [CI], 0.78-1.36), these injuries were associated with 33% higher rates of graft failure (HR, 1.33; 95% CI, 1.03-1.72). Patients with serious fall injuries spent 12.1% of posttransplant follow-up hospitalized, a 3.3-fold higher rate than those without a fall, and had nearly 2-fold higher rates of skilled nursing facility utilization (HR, 1.98; 95% CI, 1.52-2.57).

Conclusions.
Serious fall injuries are independently associated with significantly greater resource requirements and lower graft survival. Further study is needed to delineate the relationship between falls and adverse outcomes in transplant and reduce the incidence and deleterious effects of these events.
The Effect of the Opioid Epidemic on Donation After Circulatory Death Transplantation Outcomes
Authors: Wanis Kerollos Nashat , Madenci Arin L. , Dokus M. Katherine , Tomiyama Koji , Al-Judaibi Bandar M. , Hernán Miguel A. , Hernandez-Alejandro Roberto 
Published: September 2018

Background.
The opioid epidemic and the deaths of otherwise healthy individuals due to drug overdose in the United States has major implications for transplantation. The current extent and safety of utilization of liver and kidney grafts from donation after circulatory death (DCD) donors who died from opioid overdose is unknown.

Methods.
Using national data from 2006 to 2016, we estimated the cumulative incidence of graft failure for recipients of DCD grafts, comparing the risk among recipients of organs from donors who died of anoxic drug overdose and recipients of organs from donors who died of other causes.

Results.
One hundred seventy-nine (6.2%) of 2908 liver graft recipients and 944 (6.1%) of 15520 kidney graft recipients received grafts from donors who died of anoxic drug overdose. Grafts from anoxic drug overdose donors were less frequently used compared with other DCD grafts (liver, 25.9% versus 29.6%; 95% confidence interval [CI] for difference, −6.7% to −0.7%; kidney, 81.0% versus 84.7%; 95% CI for difference, −7.3% to −0.1%). However, the risk of graft failure at 5 years was similar for recipients of anoxic drug overdose donor grafts and recipients of other grafts (liver risk difference, 1.8%; 95% CI, −7.8% to 11.8%; kidney risk difference, −1.5%; 95% CI, −5.4% to 3.1%).

Conclusions.
In the context of the current opioid epidemic, utilization of anoxic drug overdose DCD donor grafts does not increase the risk of graft failure and may help to address waitlist demands.
A Case of Musical Hallucinations Related to Mirtazapine
Authors: Lee Grace H. , Stewart Jonathan T. 
Published: September 2018

Abstract
Musical hallucinations (MHs) are relatively uncommon phenomena sometimes encountered in older patients, especially older women. They usually involve popular, overlearned music, either entire songs or repetitive snippets. While MHs are most commonly associated with hearing loss, they may occur in a variety of psychiatric, neurologic, and iatrogenic conditions. We report a 91-year-old man whose MHs were causally related to the antidepressant mirtazapine. Although mirtazapine is generally well tolerated, it may rarely cause MHs or other psychotic symptoms.
Tandospirone-Induced Rhabdomyolysis
Authors: Miyazaki Kensuke , Otaka Masabumi , Yasui-Furukori Norio 
Published: September 2018

Background
Rhabdomyolysis involves the release of intracellular contents secondary to muscle cell injury; it generally presents with muscle pain and weakness. Although several psychotropic agents have been documented as causes of rhabdomyolysis, there are no reports of tandospirone-induced rhabdomyolysis.

Case
We present the case of a 15-year-old Japanese girl who had posttraumatic stress disorder after the Great East Japan Earthquake. She received a dose of 60 mg of tandospirone while taking 10 mg of tandospirone and 400 mg of valproic acid every day. She developed appetite loss, muscle weakness, muscle soreness, and general malaise on day 2, and laboratory data revealed a serum creatine phosphokinase level of 17,770 IU/L that reached a peak of 35,530 IU/L on day 4. Lactate dehydrogenase, aspartate aminotransferase, and alanine transaminase levels were also abnormal. After a fluid infusion was initiated and tandospirone was discontinued, most of her symptoms and abnormal laboratory data resolved within 10 days.

Conclusion
This case suggests that careless high dosing of partial 5-HT1A receptor agonists is harmful to at-risk patients, such as adolescent patients with poor mental condition.
Levetiracetam-Induced Seizure Aggravation in Patients With Focal Cortical Dysplasia
Authors: Cvetkovska Emilija , Kuzmanovski Igor , Babunovska Marija , Boshkovski Bojan , Aleksovska Katina , Trencevska Gordana Kiteva 
Published: September 2018

Objectives
The choice of antiepileptic drug is typically based on seizure type, and there is no evidence for superior effectiveness or potential deterioration of particular antiepileptic drug in specific etiologic subgroups. The aim of the study was to identify etiological factor(s) associated with increased risk of seizure aggravation with levetiracetam (LEV).

Methods
A retrospective analysis of 139 patients treated with LEV was performed. Seizure aggravation was defined as a 100% or greater increase in seizures frequency, which occurred within 1 month of drug introduction.

Results
Five patients who fulfilled the selection criteria were identified. Seizure aggravation occurred with low doses (500–1000 mg) of LEV. In addition to increased frequency and duration, 2 patients developed new seizure types. Withdrawal of LEV resulted in seizure return to background frequency in all patients. Four of 5 patients have distinctive magnetic resonance imaging finding of focal cortical dysplasia. No patients with paradoxical effect of LEV were detected in the idiopathic epilepsy group or other types of symptomatic epilepsies.

Conclusions
Our results suggest that LEV may possibly induce seizure exacerbation in a subset of patients with focal cortical dysplasia–related epilepsy, although large studies are needed to establish the relation. Underlying causes of epilepsy could impact the treatment choice because electroclinical semiology might be the “final common pathway” of different epileptogenic mechanisms in diverse etiologies.
Increased Risk of Ischemic Stroke in Multiple Myeloma Associated With Lenalidomide Treatment: A Case Report and Review of the Literature
Authors: de Celis Elena , Alonso de Leciñana María , Rodríguez-Pardo Jorge , Fuentes Blanca , Díez-Tejedor Exuperio 
Published: September 2018

Objective
The aim of the study was to illustrate the increased risk of ischemic stroke in the context of multiple myeloma (MM) under treatment with lenalidomide combined with dexamethasone.

Methods
This is a case report and literature review.

Results
A 62-year-old woman diagnosed with relapsed MM under treatment with lenalidomide and dexamethasone presented with acute onset disorientation, disturbed behavior, and aphasia. Cranial computed tomography scan revealed an acute cerebral infarction in the left middle cerebral artery territory, and brain magnetic resonance imaging showed additional silent ischemic lesions in other arterial territories. Common stroke etiologies were excluded after an extensive study, leading to a final diagnosis of cerebral infarction of uncommon cause probably related to MM and treatment with lenalidomide plus dexamethasone. A literature review provided 84 reports from the license holder, 2 more cases of stroke in patients with MM receiving lenalidomide and a recurrent stroke in a patient experiencing polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS syndrome) treated with lenalidomide.

Conclusions
Our case exemplifies the need to raise awareness about the risk of ischemic stroke associated with MM that might be increased by treatment with lenalidomide and to establish consistent recommendations regarding thromboprophylaxis to reduce comorbidities and mortality in these patients.
Host JAK-STAT activity is a target of parasitoid wasp virulence strategies
Authors: Brantley Susanna E. , Stouthamer Corinne M. , Kr Pooja , Fischer Mary L. , Hill Joshua , Schlenke Todd A. , Mortimer Nathan T. 
Published: September 2018

AbstractInnate immune responses that allow hosts to survive infection depend on the action of multiple conserved signaling pathways. Pathogens and parasites in turn have evolved virulence factors to target these immune signaling pathways in an attempt to overcome host immunity. Consequently, the interactions between host immune molecules and pathogen virulence factors play an important role in determining the outcome of an infection. The immune responses ofDrosophila melanogasterprovide a valuable model to understand immune signaling and host-pathogen interactions. Flies are commonly infected by parasitoid wasps and mount a coordinated cellular immune response following infection. This response is characterized by the production of specialized blood cells called lamellocytes that form a tight capsule around wasp eggs in the host hemocoel. The conserved JAK-STAT signaling pathway has been implicated in lamellocyte proliferation and is required for successful encapsulation of wasp eggs. Here we show that activity ofStat92E, theD. melanogasterSTAT ortholog, is induced in immune tissues following parasitoid infection. Virulent wasp species are able to suppressStat92Eactivity during infection, suggesting they target JAK-STAT pathway activation as a virulence strategy. Furthermore, two wasp species (Leptopilina guineaensisandGanaspis xanthopoda) suppress phenotypes associated with a gain-of-function mutation inhopscotch, theD. melanogasterJAK ortholog, indicating that they inhibit the activity of the core signaling components of the JAK-STAT pathway. Our data suggest that parasitoid wasp virulence factors block JAK-STAT signaling to overcome fly immune defenses.Author SummaryFollowing infection, host immune responses are triggered to provide protection against the invading pathogen. The proper function of these responses depends on the activity of multiple immune signaling pathways. These pathways act in a coordinated manner to orchestrate the immune response, and any disruption can render the host susceptible to infection. Because of this sensitivity, many pathogen species have evolved virulence mechanisms that target host signaling pathways and disrupt their function. We are using the interaction betweenDrosophila melanogasterandDrosophila-infecting parasitoid wasps to study this relationship between host signaling and pathogen virulence. Parasitoids infect fly larvae, and during infection, transfer virulence protein containing venom into the host, providing a mechanism to alter host signaling. This study is focused on one key immune signaling pathway, the highly conserved JAK-STAT pathway. We find that many virulent parasitoid species restrict the activity of the host JAK-STAT pathway, providing a clue as to their virulence strategy. JAK-STAT signaling plays many additional roles in health and disease, and so this system provides a good model to further understand this important pathway.
GIGANTEApromotes sorghum flowering by stimulating floral activator gene expression
Authors: Harmon Frank G. , Chen Junping , Xin Zhanguo 
Published: September 2018

iv.FundingThis work was supported by USDA-ARS CRIS projects 2030-21000-039-00D and 2030-21000-049-00D to F.G.H.v.AbstractThe C4 grassSorghum bicoloris an important grain and subsistence crop, animal forage, and cellulosic biofuel feedstock that is tolerant of abiotic stresses and marginal soils. Sorghum is short-day flowering, an obstacle for adaptation as a grain crop but a benefit as a biofuel feedstock. To identify genes underlying sorghum photoperiodic flowering behavior this study characterized theSbgi-ems1nonsense mutation in the sorghumGIGANTEA(SbGI) gene from a sequenced M4 EMS-mutagenized BTx623 population.Sbgi-ems1plants had reduced stature and leaf blades exhibiting increased lateral growth combined with reduced proximal-distal growth. Mutant plants flowered later than normal siblings under long-day conditions provided by greenhouse or field. Delayed flowering inSbgi-ems1plants accompanied by an increase in internode number, indicating an extended vegetative growth phase prior to flowering.Sbgi-ems1plants had reduced expression of floral activator genesSbCOandSbEhd1and downstream FT-like florigen genesSbFT, SbCN8, andSbCN12. Therefore,SbGIaccelerates flowering by promotion ofSbCOandSbEhd1expression. Circadian clock-associated genesSbTOC1andSbLHYhad disrupted expression inSbgi-ems1plants. This work demonstratesSbGIis a key upstream activator in the regulatory networks dictating sorghum flowering time and growth, as well as gene expression regulation within the circadian clock.Summary StatementSorghumGIGANTEAcontributes to flowering time, growth, and the circadian clock with activities opposite to its maize homolog.GIoccupies a conserved position within regulatory networks but has plastic activity.
Host genetic associations with the gut microbiota in HIV-1-infected subjects: a pilot exploratory study
Authors: Guillén Yolanda , Noguera-Julian Marc , Rivera Javier , Casadellà Maria , Rocafort Muntsa , Parera Mariona , Mothe Beatriz , Coll Josep , Saz Jorge , Navarro Jordi , Crespo Manuel , Negredo Eugènia , Brander Christian , Calle Maria Luz , Clotet Bonaventura , Paredes Roger 
Published: September 2018

AbstractThe impact of host genetics on gut microbial dynamics is debated. No study to date has investigated the possible role of host genetics in shaping the gut microbiota in HIV-1 infected subjects. With the aim of generating preliminary data to inform future host genetic studies, we performed an exploratory host exome analysis of 147 subjects either infected or at risk of becoming infected with HIV-1 from the MetaHIV cohort in Barcelona. Using a DNA microarray chip, we sought to identify host genetic variants associated to three specific microbial features with a potentially inheritable component, and which were previously found to be associated with gut dysbiosis in HIV infection, i.e.: gut enterotype, presence of methanogenic archaea and microbial gene richness. After correction for multiple comparisons, we did not observe any statistically significant association between the host’s genetic landscape and the explored gut microbiome traits. These findings will help design future, adequately-powered studies to assess the influence of host genetics in the microbiome of HIV-1-infected subjects.
Inhibition of the amino-acid transporter LAT1 demonstrates anti-neoplastic activity in medulloblastoma
Authors: Cormerais Yann , Pagnuzzi-Boncompagni Marina , Schrötter Sandra , Giuliano Sandy , Tambutté Eric , Endou Hitoshi , Wempe Michael F. , Pagès Gilles , Pouysségur Jacques , Picco Vincent 
Published: September 2018

ABSTRACTMost cases of medulloblastoma (MB) occur in young children. While the overall survival rate can be relatively high, current treatments combining surgery, chemo- and radiotherapy are very destructive for patient development and quality of life. Moreover, aggressive forms and recurrences of MB cannot be controlled by classical therapies. Therefore, new therapeutic approaches yielding good efficacy and low toxicity for healthy tissues are required to improve patient outcome. Cancer cells sustain their proliferation by optimizing their nutrient uptake capacities. The L-type amino acid transporter 1 (LAT1) is an essential amino acid carrier overexpressed in aggressive human cancers that was described as a potential therapeutic target. In this study, we investigated the therapeutic potential of JPH203, a LAT1-specific pharmacological inhibitor, on two independent MB cell lines belonging to subgroups 3 (HD-MB03) and Shh (DAOY). We show that while displaying low toxicity towards normal cerebral cells, JPH203 disrupts AA homeostasis, mTORC1 activity, proliferation and survival in MB cells. Moreover, we demonstrate that a long-term treatment with JPH203 does not lead to resistance in MB cells. Therefore, the present study suggests that targeting LAT1 with JPH203 is a promising therapeutic approach for MB treatment.
Leveraging brain cortex-derived molecular data to elucidate epigenetic and transcriptomic drivers of neurological function and disease
Authors: Hatcher Charlie , Relton Caroline L. , Gaunt Tom R. , Richardson Tom G. 
Published: September 2018

AbstractIntegrative approaches which harness large-scale molecular datasets can help develop mechanistic insight into findings from genome-wide association studies (GWAS). We have performed extensive analyses to uncover transcriptional and epigenetic processes which may play a role in neurological trait variation.This was undertaken by applying Bayesian multiple-trait colocalization systematically across the genome to identify genetic variants responsible for influencing intermediate molecular phenotypes as well as neurological traits. In this analysis we leveraged high dimensional quantitative trait loci data derived from prefrontal cortex tissue (concerning gene expression, DNA methylation and histone acetylation) and GWAS findings for 5 neurological traits (Neuroticism, Schizophrenia, Educational Attainment, Insomnia and Alzheimer’s disease).There was evidence of colocalization for 118 associations suggesting that the same underlying genetic variant influenced both nearby gene expression as well as neurological trait variation. Of these, 73 associations provided evidence that the genetic variant also influenced proximal DNA methylation and/or histone acetylation. These findings support previous evidence at loci where epigenetic mechanisms may putatively mediate effects of genetic variants on traits, such as KLC1 and schizophrenia. We also uncovered evidence implicating novel loci in neurological disease susceptibility, including genes expressed predominantly in brain tissue such as MDGA1, KIRREL3 and SLC12A5.An inverse relationship between DNA methylation and gene expression was observed more than can be accounted for by chance, supporting previous findings implicating DNA methylation as a transcriptional repressor. Our study should prove valuable in helping future studies prioritise candidate genes and epigenetic mechanisms for in-depth functional follow-up analyses.
Identification of a novel deltavirus in Boa constrictor
Authors: Hetzel Udo , Szirovicza Leonóra , Smura Teemu , Prähauser Barbara , Vapalahti Olli , Kipar Anja , Hepojoki Jussi 
Published: September 2018

AbstractHuman hepatitis D virus (hHDV) forms the genus Deltavirus which has not been assigned to any virus family. hHDV is a satellite virus and needs hepatitis B virus (HBV) to make infectious particles. Deltaviruses are thought to have evolved in humans, since they have thus far not been identified elsewhere. Herein we report, prompted by a recent observation of HDV-like agent in birds, the identification of a deltavirus in a snake (Boa constrictor) designated as snake-HDV (sHDV). The circular 1711 nt RNA genome of the newly identified virus resembles hHDV in its coding strategy and size. We discovered sHDV when performing a meta-transcriptomic study on brain samples of two boas with central nervous system signs. We did not identify accompanying HBV-like sequences in the samples. By sequence comparison, the putative hepatitis D antigen (HDAg) of sHDV, encoded by one of the two open reading frames (ORFs), is roughly 50% identical to the previously known HDAgs. We used antiserum raised against recombinant snake HDAg to demonstrate a broad viral target cell spectrum, ranging from neurons over epithelial cells to leukocytes. Using RT-PCR, we detected sHDV RNA also in the liver and blood of the two snakes and could show sHDV infection not only in two of their juvenile offspring, but also in a water python (Liasis mackloti savuensis) in the same snake colony, indicating potentially vertical and horizontal transmission. The finding of abundant sHDAg in several tissues suggests that sHDV actively replicated in the studied animals. Our findings suggest that sHDV spread may not be restricted to hepadnavirus co-infection. This would imply that deltaviruses may employ other enveloped viruses for producing infectious particles.
Impaired cognitive performance under psycho-social stress in cannabis-dependent males is mediated by attenuated precuneus activity
Authors: Zhao Weihua , Zimmermann Kaeli , Zhou Xinqi , Zhou Feng , Fu Meina , Dernbach Christian , Scheele Dirk , Weber Bernd , Eckstein Monika , Hurlemann René , Kendrick Keith M , Becker Benjamin 
Published: September 2018

AbstractBackgroundDeficient regulation of stress plays an important role in the escalation of substance use, addiction and relapse. Accumulating evidence suggests dysregulations in cognitive and reward-related processes and the underlying neural circuitry in cannabis dependence. However, despite the important regulatory role of the endocannabinoid system in the stress response, associations between chronic cannabis use and altered stress processing on the neural level have not been systematically examined.MethodsAgainst this background, the present functional magnetic resonance imaging (fMRI)study examined psycho-social stress processing in cannabis-dependent males (n = 28) and matched controls (n = 23) using an established stress-induction paradigm (Montreal Imaging Stress Task) that combines computerized (adaptive) mental arithmetic challenges with social evaluative threat.ResultsDuring psycho-social stress exposure, but not the no-stress condition, cannabis users demonstrated impaired performance relative to controls. In contrast, levels of experienced stress and cardiovascular stress responsivity did not differ from controls. Functional MRI data revealed that stress-induced performance deteriorations in cannabis users were accompanied by decreased precuneus activity and increased connectivity of this region with the dorsal medial prefrontal cortex.LimitationsOnly male cannabis-dependent users were examined, the generalizability in female users remains to be determined.ConclusionTogether, the present findings provide first evidence for exaggerated stress-induced cognitive performance deteriorations in cannabis users. The neural data suggest that deficient stress-related dynamics of the precuneus may mediate the deterioration of performance on the behavioral level.