bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amyloid‐beta1–42 induced glutamatergic receptor and transporter expression changes in the mouse hippocampus
Authors: Yeung Jason H.Y. , Calvo‐Flores Guzmán Beatriz , Palpagama Thulani H. , Ethiraj Jayarjun , Zhai Ying , Tate Warren P. , Peppercorn Katie , Waldvogel Henry J. , Faull Richard L.M. , Kwakowsky Andrea 
Published: June 2020

AbstractAlzheimer's disease (AD) is the leading type of dementia worldwide. With an increasing burden of an aging population coupled with the lack of any foreseeable cure, AD warrants the current intense research effort on the toxic effects of an increased concentration of beta‐amyloid (Aβ) in the brain. Glutamate is the main excitatory brain neurotransmitter and it plays an essential role in the function and health of neurons and neuronal excitability. While previous studies have shown alterations in expression of glutamatergic signaling components in AD, the underlying mechanisms of these changes are not well understood. This is the first comprehensive anatomical study to characterize the subregion‐ and cell layer‐specific long‐term effect of Aβ1–42 on the expression of specific glutamate receptors and transporters in the mouse hippocampus, using immunohistochemistry with confocal microscopy. Outcomes are examined 30 days after Aβ1–42 stereotactic injection in aged male C57BL/6 mice. We report significant decreases in density of the glutamate receptor subunit GluA1 and the vesicular glutamate transporter (VGluT) 1 in the conus ammonis 1 region of the hippocampus in the Aβ1–42 injected mice compared with artificial cerebrospinal fluid injected and naïve controls, notably in the stratum oriens and stratum radiatum. GluA1 subunit density also decreased within the dentate gyrus dorsal stratum moleculare in Aβ1–42 injected mice compared with artificial cerebrospinal fluid injected controls. These changes are consistent with findings previously reported in the human AD hippocampus. By contrast, glutamate receptor subunits GluA2, GluN1, GluN2A, and VGluT2 showed no changes in expression. These findings indicate that Aβ1–42 induces brain region and layer specific expression changes of the glutamatergic receptors and transporters, suggesting complex and spatial vulnerability of this pathway during development of AD neuropathology.
image
Read the Editorial Highlight for this article on page 7.Cover Image for this issue: https://doi.org/10.1111/jnc.14763.
Transcranial Doppler Emboli Monitoring for Infective Endocarditis
Authors: Huang Glen , Johnson Leilani L. , Peacock James E. , Tegeler Charles , Davis Kyle , Sarwal Aarti 
Published: June 2020

ABSTRACTBACKGROUND AND PURPOSEIschemic stroke can occur in 20‐55% of patients with infective endocarditis (IE) with 75% occurring during the first 2 weeks of treatment. CT or MRI brain can diagnose the sequelae of stroke but transcranial Doppler (TCD) can document active embolization. We undertook a retrospective review of our patient cohort and a systematic review of literature to assess the role of TCD in early diagnosis and management of ischemic stroke in IE.METHODSRetrospective chart review and literature review.RESULTSWe found 89 patients with stroke caused by IE at our institution from December 2011 to April 2018. TCDs were obtained on 26 patients; 16 were abnormal for cerebrovascular abnormalities. Only 4 patients had 30‐minute emboli monitoring performed, of which one revealed emboli. We found 3 studies investigating the role of TCDs in IE that showed promise in its use as a predictive tool in stroke risk stratification.CONCLUSIONSPresence of embolization in the form of high‐intensity transient signals (HITS) detected on TCDs can be used for early diagnosis of IE, assessing efficacy of antibiotic therapy, and stratification of stroke risk in IE. This can aid further research into testing preventative interventions for reducing stroke burden in IE such as earlier valvular surgery or vacuum‐assisted vegetation extraction.
KRAS mutations in brown tumor of the jaws in hyperparathyroidism
Authors: Guimarães Letícia Martins , Gomes Isadora Pereira , Pereira Thaís dos Santos Fontes , de Andrade Bruno Augusto Benevenuto , Romañach Mário José , de Lacerda Júlio César Tanos , Pontes Hélder Antônio Rebelo , Brennan Peter A. , Rahimi Siavash , Carlos Román , Mosqueda‐Taylor Adalberto , Bologna‐Molina Ronell , Passador‐Santos Fabricio , Gomez Ricardo Santiago , Gomes Carolina Cavaliéri 
Published: June 2020

AbstractBackgroundBrown tumors are giant cell‐rich lesions that result from abnormal bone metabolism in hyperparathyroidism, one of the most common endocrine disorders worldwide. Brown tumors occasionally affect the jaws and, despite well‐known clinical and microscopic features, their molecular pathogenesis remains unclear. We investigated the presence of pathogenic activating mutations in TRPV4, FGFR1, and KRAS in a cohort of brown tumors since these have recently been reported in giant‐cell lesions of the jaws and non‐ossifying fibromas of the bones (FGFR1 and KRAS), which are histologic mimics of brown tumors.MethodsWe target sequenced 13 brown tumors of the jaws associated with primary or secondary hyperparathyroidism. As mutations in these genes are known to activate the MAPK/ERK signaling pathway, we also assessed the immunostaining of the phosphorylated form of ERK1/2 (pERK1/2) in these lesions.ResultsKRAS pathogenic mutations were detected in seven cases (p.G12V n = 4, p.G12D n = 1, p.G13D n = 1, p.A146T n = 1). KRAS variants of unknown significance (VUS), p.A134T and p.E37K, were also detected. All samples showed wild‐type sequences for FGFR1 and TRPV4 genes. The activation of the MAPK/ERK signaling pathway was demonstrated by pERK1/2 immunohistochemical positivity of the brown tumors´ mononuclear cells.ConclusionMutations in KRAS and activation of the MAPK/ERK signaling pathway were detected in brown tumors of hyperparathyroidism of the jaws, expanding the spectrum of giant cell lesions whose molecular pathogenesis involve RAS signaling.
Emerging zoonotic diseases originating in mammals: a systematic review of effects of anthropogenic land‐use change
Authors: White Rebekah J. , Razgour Orly 
Published: June 2020

Abstract

Zoonotic pathogens and parasites that are transmitted from vertebrates to humans are a major public health risk with high associated global economic costs. The spread of these pathogens and risk of transmission accelerate with recent anthropogenic land‐use changes (LUC) such as deforestation, urbanisation, and agricultural intensification, factors that are expected to increase in the future due to human population expansion and increasing demand for resources.

We systematically review the literature on anthropogenic LUC and zoonotic diseases, highlighting the most prominent mammalian reservoirs and pathogens, and identifying avenues for future research.

The majority of studies were global reviews that did not focus on specific taxa. South America and Asia were the most‐studied regions, while the most‐studied LUC was urbanisation. Livestock were studied more within the context of agricultural intensification, carnivores with urbanisation and helminths, bats with deforestation and viruses, and primates with habitat fragmentation and protozoa.

Research into specific animal reservoirs has improved our understanding of how the spread of zoonotic diseases is affected by LUC. The behaviour of hosts can be altered when their habitats are changed, impacting the pathogens they carry and the probability of disease spreading to humans. Understanding this has enabled the identification of factors that alter the risk of emergence (such as virulence, pathogen diversity, and ease of transmission). Yet, many pathogens and impacts of LUC other than urbanisation have been understudied.

Predicting how zoonotic diseases emerge and spread in response to anthropogenic LUC requires more empirical and data synthesis studies that link host ecology and responses with pathogen ecology and disease spread. The link between anthropogenic impacts on the natural environment and the recent COVID‐19 pandemic highlights the urgent need to understand how anthropogenic LUC affects the risk of spillover to humans and spread of zoonotic diseases originating in mammals.
The majority of the matrix protein TapA is dispensable for Bacillus subtilis colony biofilm architecture
Authors: Earl Chris , Arnaouteli Sofia , Bamford Natalie C. , Porter Michael , Sukhodub Tetyana , MacPhee Cait E. , Stanley‐Wall Nicola R. 
Published: June 2020

AbstractBiofilm formation is a co‐operative behaviour, where microbial cells become embedded in an extracellular matrix. This biomolecular matrix helps manifest the beneficial or detrimental outcome mediated by the collective of cells. Bacillus subtilis is an important bacterium for understanding the principles of biofilm formation. The protein components of the B. subtilis matrix include the secreted proteins BslA, which forms a hydrophobic coat over the biofilm, and TasA, which forms protease‐resistant fibres needed for structuring. TapA is a secreted protein also needed for biofilm formation and helps in vivo TasA‐fibre formation but is dispensable for in vitro TasA‐fibre assembly. We show that TapA is subjected to proteolytic cleavage in the colony biofilm and that only the first 57 amino acids of the 253‐amino acid protein are required for colony biofilm architecture. Through the construction of a strain which lacks all eight extracellular proteases, we show that proteolytic cleavage by these enzymes is not a prerequisite for TapA function. It remains unknown why TapA is synthesised at 253 amino acids when the first 57 are sufficient for colony biofilm structuring; the findings do not exclude the core conserved region of TapA having a second role beyond structuring the B. subtilis colony biofilm.
Relationship between the location of ligamentum flavum hypertrophy and its stress in finite element analysis
Authors: Peng Yong‐xing , Zheng Zhen‐yu , Wang, MD Wei‐guo , Liu Lin , Chen, MD Feng , Xu, MD Hong‐tao , Zhang Zhong‐min 
Published: June 2020

ObjectiveTo quantitatively describe the stress of the ligamentum flavum (LF) using the finite element method and to compare the stress at different parts of the healthy LF.MethodsBased on the high resolution computed tomography imaging data of a healthy 22‐year‐old man, three‐dimensional nonlinear L4–5 lumbar finite element model (FEM) representing intact condition was developed. The LF, as the object of the present research, was incorporated into the spinal model in the form of solid three‐dimensional structure. The model’s validity is verified by comparing its biomechanical indices, such as range of motion and axial compression pressure displacement, with published results under specific loading conditions. To authenticate the accuracy of the solid LF, the lamina attachments, the central cross‐section, and other anatomy indicators were compared with figures in the published literature. After the average and maximum von Mises stress on the surface of LF under various working conditions were measured using ANSYS and AutoCAD software, the surface stress difference in the LF between the ventral and dorsal sides as well as the lateral and lamina parts were determined.ResultsThe FEM predicted a similar tendency for biomechanical indices as shown in previous studies. The lamina attachments, the central cross‐section, and the height as well as the width of the LF in the healthy FEM were in accordance with published results. In the healthy model, the average and maximum von Mises stress in the shallow layer of the LF were, respectively, 1.40, 2.28, 1.76, 1.48, 1.38 and 1.79, 2.41, 1.46, 1.42, 1.71 times that in the deep layer under a compressive preload of 500 N incorporated with flexion, extension, and lateral and rotational moments (10 Nm). The most conspicuous difference in surface stress was observed with the flexion motion, with a nearly 241% difference in the maximum stress and a 228% difference in the average stress compared to those in other states. As far as the whole dorsal side of the LF was concerned, the maximum surface stress was almost all concentrated in the dorsal neighboring facet joint portion. In addition, the maximum and average stress were, respectively, 77%, 72%, 15%, 11%, 71% and 153%, 39%, 54%, 200%, 212% higher in the lateral part than in the lamina part.ConclusionBased on the predisposition of LF hypertrophy in the human spine and the stress distribution of this study, the positive correlation between LF hypertrophy and its stress was confirmed.
The potential for Fusarium oxysporum f. sp. fragariae, cause of fusarium wilt of strawberry, to colonize organic matter in soil and persist through anaerobic soil disinfestation
Authors: Henry Peter M. , Haugland Megan , Lopez Lia , Munji Mariel , Watson Dean C. , Gordon Thomas R. 
Published: June 2020

AbstractFusarium wilt of strawberry, caused by Fusarium oxysporum f. sp. fragariae, is a disease of primary concern for strawberry production in many countries. Crop rotation and anaerobic soil disinfestation (ASD) have gained recent interest for their potential to contribute to management of this disease. Both techniques involve incorporation of organic matter into soil, which may be utilized by strains of Fusarium that are competitive saprophytes. We show that F. oxysporum f. sp. fragariae can colonize strawberry, lettuce, raspberry, and broccoli leaf tissues, which are sources of organic matter generated during crop rotation. This pathogen increased in soil population density during ASD treatments that did not become anaerobic, possibly as a result of growth on the organic amendment. However, significant population decreases were observed after ASD treatment when at least 100,000 cumulative reduced mV hours occurred in a 14‐day experiment. Post‐ASD abundance of F. oxysporum f. sp. fragariae in soil was negatively correlated with cumulative reduced mV hours. The only treatment that consistently caused disinfestation was exposed to a maximum temperature of 22 °C, which indicates there is potential for developing effective ASD treatments in the cool climates where strawberries are grown. Awareness that F. oxysporum f. sp. fragariae can act as a competitive soil saprophyte should be further investigated for its potential to alter disease outcomes where organic amendments are applied.
Neurodevelopmental findings in children 20‐30 months of age with postnatal Zika infection at 1‐12 months of age, Colombia, September‐November 2017
Authors: Pacheco Oscar , Newton Suzanne M. , Daza Marcela , Cates Jordan E. , Reales Javier Alberto Madero , Burkel Veronica K. , Mercado Marcela , Godfred‐Cato Shana , Gonzalez Maritza , Anderson Kayla N. , Woodworth Kate R. , Valencia Diana , Tong Van T. , Gilboa Suzanne M. , Osorio May Bibiana , Rodríguez Dora Yurany Sánchez , Prieto‐Alvarado Franklyn Edwin , Moore Cynthia A. , Honein Margaret A. , Ospina Martínez Martha L. 
Published: June 2020

AbstractBackgroundZika virus (ZIKV) infection during pregnancy can cause infant brain and eye abnormalities and has been associated with adverse neurodevelopmental outcomes in exposed infants. Evidence is limited on ZIKV’s effects on children infected postnatally within the first year of life.ObjectiveTo determine whether any adverse neurodevelopmental outcomes occurred in early childhood for children infected postnatally with ZIKV during infancy, given the neurotoxicity of ZIKV infection and the rapid brain development that occurs in infancy and early childhood.MethodsThe Colombia Instituto Nacional de Salud (INS) conducted health and developmental screenings between September and November 2017 to evaluate 60 children at ages 20‐30 months who had laboratory‐confirmed symptomatic postnatal ZIKV infection at ages 1‐12 months. We examined the frequency of adverse neurologic, hearing, eye, and developmental outcomes as well as the relationship between age at Zika symptom onset and developmental outcomes.ResultsNine of the 60 (15.0%) children had adverse outcomes on the neurologic, hearing, or eye examination. Six of the 47 (12.8%) children without these adverse findings, and who received a valid developmental screening, had an alert score in the hearing‐language domain which signals the need for additional developmental evaluation.ConclusionNeurologic, hearing, eye, and developmental findings suggest reassuring results. Since the full spectrum of neurodevelopmental outcomes in children postnatally infected with ZIKV remains unknown, routine paediatric care is advised to monitor the development of these children to ensure early identification of any adverse neurodevelopmental outcomes.
The epidemiology of kicking injuries in professional Rugby Union: A 15‐season prospective study
Authors: Lazarczuk Stephanie L. , Love Thomas , Cross Matthew J. , Stokes Keith A. , Williams Sean , Taylor Aileen E. , Fuller Colin W. , Brooks John H. M. , Kemp Simon P. T. , Bezodis Neil E. 
Published: June 2020

PurposeWhile kicking in Rugby Union can be influential to match outcome, the epidemiology of kicking injuries remains unknown. This study therefore aimed to investigate the epidemiology of injuries attributed to kicking in professional rugby, including playing position‐specific effects and differences in kicking volumes and kick types.MethodsFifteen seasons of injury surveillance data and two seasons of match kicking characteristics from professional rugby players were analyzed. Incidence, propensity, and severity of kicking‐related injuries were calculated together with the locations and types of these injuries. Position‐related differences in match kicking types and volumes were also established.ResultsSeventy‐seven match and 55 training acute‐onset kicking injuries were identified. The match kicking injury incidence for backs was 1.4/1000 player‐match‐hours. Across all playing positions, the propensity for match kicking injury was 0.57 injuries/1000 kicks. Fly‐halves sustained the greatest proportion of match kicking injuries (47%) and performed the greatest proportion of match kicks (46%); an average propensity for match kicking injury (0.58/1000 kicks). Scrum‐halves executed 27% of match‐related kicks but had a very low propensity for match kicking injury (0.17/1000 kicks). All other positional groups executed a small proportion of match‐related kicks but a high propensity for match kicking injury. Ninety‐two percent of match kicking injuries occurred in the pelvis or lower limb, with the majority sustained by the kicking limb. 21% of all match kicking injuries were associated with the rectus femoris muscle.ConclusionMatch kicking profiles and kicking injuries sustained are position‐dependent, which provides valuable insight for developing player‐specific conditioning and rehabilitation protocols.
Supersymmetric Dirac Hamiltonians in ($$1+1$$) dimensions revisited
Authors: Junker Georg 
Published: June 2020

AbstractThe most general Dirac Hamiltonians in $$(1+1)$$

(
1
+
1
)

dimensions are revisited under the requirement to exhibit a supersymmetric structure. It is found that supersymmetry allows either for a scalar or a pseudo-scalar potential. Their spectral properties are shown to be represented by those of the associated non-relativistic Witten model. The general discussion is extended to include the corresponding relativistic and non-relativistic resolvents. As example, the well-studied relativistic Dirac oscillator is considered and the associated resolved kernel is found in a closed-form expression by utilising the energy-dependent Green’s function of the non-relativistic harmonic oscillator. The supersymmetric quasi-classical approximation for the Witten model is extended to the associated relativistic model.
Linear eigenvalue statistics of random matrices with a variance profile
Authors: Adhikari Kartick , Jana Indrajit , Saha Koushik 
Published: June 2020

We give an upper bound on the total variation distance between the linear eigenvalue statistic, properly scaled and centered, of a random matrix with a variance profile and the standard Gaussian random variable. The second-order Poincaré inequality-type result introduced in [S. Chatterjee, Fluctuations of eigenvalues and second order poincaré inequalities, Prob. Theory Rel. Fields 143(1) (2009) 1–40.] is used to establish the bound. Using this bound, we prove central limit theorem for linear eigenvalue statistics of random matrices with different kind of variance profiles. We re-establish some existing results on fluctuations of linear eigenvalue statistics of some well-known random matrix ensembles by choosing appropriate variance profiles.
Stromal CAVIN1 Controls Prostate Cancer Microenvironment and Metastasis by Modulating Lipid Distribution and Inflammatory Signaling
Authors: Low Jin-Yih , Brennen W. Nathaniel , Meeker Alan K. , Ikonen Elina , Simons Brian W. , Laiho Marikki 
Published: June 2020

Abstract

Lipid uptake occurs through caveolae, plasma membrane invaginations formed by caveolins (CAV) and caveolae-associated protein 1 (CAVIN1). Genetic alterations of CAV1N1 and CAV1 modify lipid metabolism and underpin lipodystrophy syndromes. Lipids contribute to tumorigenesis by providing fuel to cancer metabolism and supporting growth and signaling. Tumor stroma promotes tumor proliferation, invasion, and metastasis, but how stromal lipids influence these processes remain to be defined. Here, we show that stromal CAVIN1 regulates lipid abundance in the prostate cancer microenvironment and suppresses metastasis. We show that depletion of CAVIN1 in prostate stromal cells markedly reduces their lipid droplet accumulation and increases inflammation. Stromal cells lacking CAVIN1 enhance prostate cancer cell migration and invasion. Remarkably, they increase lipid uptake and M2 inflammatory macrophage infiltration in the primary tumors and metastasis to distant sites. Our data support the concept that stromal cells contribute to prostate cancer aggressiveness by modulating lipid content and inflammation in the tumor microenvironment.

Implications:
This study showed that stromal CAVIN1 suppresses prostate cancer metastasis by modulating tumor microenvironment, lipid content, and inflammatory response.
Baseline Serum Bilirubin and Risk of First Stroke in Hypertensive Patients
Authors: Wang Jiancheng , Zhang Xianglin , Zhang Zhuxian , Zhang Yuanyuan , Zhang Jingping , Li Huan , Li Youbao , Wang Binyan , Nie Jing , Liang Min , Wang Guobao , Cai Yefeng , Li Jianping , Zhang Yan , Huo Yong , Cui Yimin , Xu Xiping , Qin Xianhui 
Published: June 2020

Background
Data on the association between serum bilirubin and the risk of stroke are limited and inconclusive. We aimed to evaluate the association between serum bilirubin and the risk of first stroke and to examine any possible effect modifiers in hypertensive patients.

Methods and Results
Our study was a post hoc analysis of the CSPPT (China Stroke Primary Prevention Trial). A total of 19 906 hypertensive patients were included in the final analysis. Cox proportional hazards models were used to estimate the hazard ratios (HRs) and 95% CIs for the risk of first stroke associated with serum bilirubin levels. The median follow‐up period was 4.5 years. When serum total bilirubin was assessed as tertiles, the adjusted HR of first ischemic stroke for participants in tertile 3 (12.9–34.1 μmol/L) was 0.75 (95% CI, 0.59–0.96), compared with participants in tertile 1 (<9.3 μmol/L). When direct bilirubin was assessed as tertiles, a significantly lower risk of first ischemic stroke was also found in participants in tertile 3 (2.5–24.8 μmol/L) (adjusted HR, 0.77; 95% CI, 0.60–0.98), compared with those in tertile 1 (<1.6 μmol/L). However, there was no significant association between serum total bilirubin (tertile 3 versus 1: adjusted HR, 1.45; 95% CI, 0.89–2.35) or direct bilirubin (tertile 3 versus 1: adjusted HR, 1.27; 95% CI, 0.76–2.11) and first hemorrhagic stroke.

Conclusions
In this sample of Chinese hypertensive patients, there was a significant inverse association between serum total bilirubin or direct bilirubin and the risk of first ischemic stroke.