bluuebunny/crossref_metadata_2025_split huggingface dataset:
QTL mapping for stripe rust and powdery mildew resistance in Triticum durum–Aegilops speltoides backcross introgression lines
Authors: Dhillon Guriqbal Singh , Kaur Satinder , Das Niranjan , Singh Rohtas , Poland Jesse , Kaur Jaspal , Chhuneja Parveen 
Published: August 2020

AbstractWheat, a major food crop, faces significant yield constraints due to losses caused by various diseases, especially rusts and powdery mildew. Since the causal organisms are always evolving, there is a never-ending hunt for new genes/quantitative trait loci (QTLs) for resistance to control the damage. For this purpose, Triticum durum–Aegilops speltoides backcross introgression lines (DS-BILs) developed in our wide hybridization programme were screened against stripe rust and powdery mildew at both seedling and adult plant stages. DS-BILs showed complete to moderate resistance at the adult plant stage while varying resistance and susceptibility at the seedling stage. A total of 1095 single-nucleotide polymorphisms (SNPs) identified on 14 chromosomes of T. durum, using genotyping by sequencing, were used for QTL mapping. Eleven unique QTLs, across six chromosomes (chr1B, chr2A, chr2B, chr3B, chr6B and chr7B) were identified for resistance, four QTLs for field mixture of stripe rust pathotypes, two QTLs for stripe rust pathotype 78S84 and five QTLs for field mixture of powdery mildew pathotypes using stepwise regression-based likelihood ratio test for additive effect of markers and single-marker analysis. Eleven DS-BILs carrying multiple QTLs were identified which will serve as a useful resource to transfer the respective resistance to susceptible cultivars to develop all stage resistant elite cultivars where QTL for stripe rust resistance QYrAs.pau-2A.1 (LOD 3.8, PVE 24.51 linked to SNP S2A_16016633) and QTL for powdery mildew resistance QPmAs.pau-6B (logarithm of the odds (LOD) 3.2, phenotypic variation explained (PVE) 17.75 linked to SNP S6B_26793381) are major targets of the transfer.
“I'm Just an Armless Guitarist”: Tony Melendez, Disability, and the Social Construction of Virtuosity
Authors: VANDERHAMM DAVID 
Published: August 2020

AbstractIn 1987, Tony Melendez—a guitarist born without arms who plays the instrument with his feet—played at a youth rally for Pope John Paul II. Immediately after his performance, the Pope kissed Melendez and instructed him to continue “giving hope” through his music. Although the guitar accompaniment of confessional, singer-songwriter music is rarely considered virtuosic, Tony Melendez's bodily difference makes his ability to sonically pass as what he calls a “common player” an impactful display of skill for his audiences. Because Melendez's body is treated as simultaneously virtuosic and disabled, his example foregrounds the social construction of both categories and challenges the tendency to isolate either in the individual body. Rather than suggesting a sort of qualified approach to “disabled” virtuosity, this article argues that there is no such thing as unqualified virtuosity. The presumed limitations and possibilities of bodies, instruments, and repertoires always inform our understandings of skill, but we are not always explicitly aware of them. Through interviews and analysis of his performances and their media representations, I show how bodily difference and the complex subject positions of both performers and audiences contribute to what counts as skill, creative labor, and agency within a particular context.
The association between menarche and myopia and its interaction with related risk behaviors among Chinese school-aged girls: a nationwide cross-sectional study
Authors: Xu Rongbin , Jan Catherine , Song Yi , Dong Yanhui , Hu Peijin , Ma Jun , Stafford Randall S. 
Published: August 2020

AbstractNearly 80% of new cases of myopia arise between 9 and 13 years old when puberty development also progresses rapidly. However, little is known about the association between myopia and puberty. We aim to evaluate the association between myopia and menarche, the most important puberty indicator for girls, and to test whether menarche could modify the effects of myopia-related behaviors. The participants came from two consecutive national surveys conducted in 30 provinces in mainland China in 2010 and 2014. We included 102,883 girls (61% had experienced menarche) aged 10–15 years. Risk behaviors for myopia which included sleep duration, homework time, and outdoor activity were measured by self-administrated questionnaire. Myopia was defined according to a validated method, and its relationships with menarche status and behaviors were evaluated by robust Poisson regression models based on generalized estimated equation adjusting for cluster effect of school. We found that postmenarche girls were at 13% (95% confidence interval: 11%–16%) higher risk of myopia than premenarche girls, after adjusting for exact age, urban–rural location, survey year, and four behavioral covariates. Short sleep duration (<7 h/d), long homework time (>1 h/d) and low frequency of weekend outdoor activity tended to be stronger (with higher prevalence ratios associated with myopia) risk factors for myopia in postmenarche girls than in premenarche girls, and their interaction with menarche status was all statistically significant (P< 0.05). Overall, our study suggests that menarche onset may be associated with increased risk of myopia among school-aged girls and could also enhance girls’ sensitivity to myopia-related risk behaviors.
The M-CSF receptor in osteoclasts and beyond
Authors: Mun Se Hwan , Park Peter Sang Uk , Park-Min Kyung-Hyun 
Published: August 2020

AbstractColony-stimulating factor 1 receptor (CSF1R, also known as c-FMS) is a receptor tyrosine kinase. Macrophage colony-stimulating factor (M-CSF) and IL-34 are ligands of CSF1R. CSF1R-mediated signaling is crucial for the survival, function, proliferation, and differentiation of myeloid lineage cells, including osteoclasts, monocytes/macrophages, microglia, Langerhans cells in the skin, and Paneth cells in the intestine. CSF1R also plays an important role in oocytes and trophoblastic cells in the female reproductive tract and in the maintenance and maturation of neural progenitor cells. Given that CSF1R is expressed in a wide range of myeloid cells, altered CSF1R signaling is implicated in inflammatory, neoplastic, and neurodegenerative diseases. Inhibiting CSF1R signaling through an inhibitory anti-CSF1R antibody or small molecule inhibitors that target the kinase activity of CSF1R has thus been a promising therapeutic strategy for those diseases. In this review, we cover the recent progress in our understanding of the various roles of CSF1R in osteoclasts and other myeloid cells, highlighting the therapeutic applications of CSF1R inhibitors in disease conditions.
Machine-learning classification using neuroimaging data in schizophrenia, autism, ultra-high risk and first-episode psychosis
Authors: Yassin Walid , Nakatani Hironori , Zhu Yinghan , Kojima Masaki , Owada Keiho , Kuwabara Hitoshi , Gonoi Wataru , Aoki Yuta , Takao Hidemasa , Natsubori Tatsunobu , Iwashiro Norichika , Kasai Kiyoto , Kano Yukiko , Abe Osamu , Yamasue Hidenori , Koike Shinsuke 
Published: August 2020

AbstractNeuropsychiatric disorders are diagnosed based on behavioral criteria, which makes the diagnosis challenging. Objective biomarkers such as neuroimaging are needed, and when coupled with machine learning, can assist the diagnostic decision and increase its reliability. Sixty-four schizophrenia, 36 autism spectrum disorder (ASD), and 106 typically developing individuals were analyzed. FreeSurfer was used to obtain the data from the participant’s brain scans. Six classifiers were utilized to classify the subjects. Subsequently, 26 ultra-high risk for psychosis (UHR) and 17 first-episode psychosis (FEP) subjects were run through the trained classifiers. Lastly, the classifiers’ output of the patient groups was correlated with their clinical severity. All six classifiers performed relatively well to distinguish the subject groups, especially support vector machine (SVM) and Logistic regression (LR). Cortical thickness and subcortical volume feature groups were most useful for the classification. LR and SVM were highly consistent with clinical indices of ASD. When UHR and FEP groups were run with the trained classifiers, majority of the cases were classified as schizophrenia, none as ASD. Overall, SVM and LR were the best performing classifiers. Cortical thickness and subcortical volume were most useful for the classification, compared to surface area. LR, SVM, and DT’s output were clinically informative. The trained classifiers were able to help predict the diagnostic category of both UHR and FEP Individuals.
The association of PTSD symptom severity with amygdala nuclei volumes in traumatized youths
Authors: Ousdal Olga Therese , Milde Anne Marita , Hafstad Gertrud Sofie , Hodneland Erlend , Dyb Grete , Craven Alexander R. , Melinder Annika , Endestad Tor , Hugdahl Kenneth 
Published: August 2020

AbstractThe amygdala is a core component in neurobiological models of stress and stress-related pathologies, including post-traumatic stress disorder (PTSD). While numerous studies have reported increased amygdala activity following traumatic stress exposure and in PTSD, the findings regarding amygdala volume have been mixed. One reason for these mixed findings may be that the amygdala has been considered as a homogenous entity, while it in fact consists of several nuclei with unique cellular and connectivity profiles. Here, we investigated amygdala nuclei volumes of the basolateral and the centrocorticomedial complex in relation to PTSD symptom severity in 47 young survivors from the 2011 Norwegian terror attack 24–36 months post-trauma. PTSD symptoms were assessed 4–5, 14–15 and 24–36 months following the trauma. We found that increased PTSD symptom severity 24–36 months post-trauma was associated with volumetric reductions of all basolateral as well as the central and the medial nuclei. However, only the lateral nucleus was associated with longitudinal symptom development, and mediated the association between 4–5 months and 24–36 months post-trauma symptoms. The results suggest that the amygdala nuclei may be differentially associated with cross-sectional and longitudinal measures of PTSD symptom severity. As such, investigations of amygdala total volume may not provide an adequate index of the association between amygdala and stress-related mental illness.
Developmental exposure to near roadway pollution produces behavioral phenotypes relevant to neurodevelopmental disorders in juvenile rats
Authors: Berg Elizabeth L. , Pedersen Lauren R. , Pride Michael C. , Petkova Stela P. , Patten Kelley T. , Valenzuela Anthony E. , Wallis Christopher , Bein Keith J. , Wexler Anthony , Lein Pamela J. , Silverman Jill L. 
Published: August 2020

AbstractEpidemiological studies consistently implicate traffic-related air pollution (TRAP) and/or proximity to heavily trafficked roads as risk factors for developmental delays and neurodevelopmental disorders (NDDs); however, there are limited preclinical data demonstrating a causal relationship. To test the effects of TRAP, pregnant rat dams were transported to a vivarium adjacent to a major freeway tunnel system in northern California where they were exposed to TRAP drawn directly from the face of the tunnel or filtered air (FA). Offspring remained housed under the exposure condition into which they were born and were tested in a variety of behavioral assays between postnatal day 4 and 50. To assess the effects of near roadway exposure, offspring of dams housed in a standard research vivarium were tested at the laboratory. An additional group of dams was transported halfway to the facility and then back to the laboratory to control for the effect of potential transport stress. Near roadway exposure delayed growth and development of psychomotor reflexes and elicited abnormal activity in open field locomotion. Near roadway exposure also reduced isolation-induced 40-kHz pup ultrasonic vocalizations, with the TRAP group having the lowest number of call emissions. TRAP affected some components of social communication, evidenced by reduced neonatal pup ultrasonic calling and altered juvenile reciprocal social interactions. These findings confirm that living in close proximity to highly trafficked roadways during early life alters neurodevelopment.
A bioenergetic shift is required for spermatogonial differentiation
Authors: Chen Wei , Zhang Zhaoran , Chang Chingwen , Yang Zhichang , Wang Pengxiang , Fu Haihui , Wei Xiao , Chen Eric , Tan Suxu , Huang Wen , Sun Liangliang , Ni Ting , Yang Yi , Wang Yuan 
Published: August 2020

AbstractA bioenergetic balance between glycolysis and mitochondrial respiration is particularly important for stem cell fate specification. It however remains to be determined whether undifferentiated spermatogonia switch their preference for bioenergy production during differentiation. In this study, we found that ATP generation in spermatogonia was gradually increased upon retinoic acid (RA)-induced differentiation. To accommodate this elevated energy demand, RA signaling concomitantly switched ATP production in spermatogonia from glycolysis to mitochondrial respiration, accompanied by increased levels of reactive oxygen species. Disrupting mitochondrial respiration significantly blocked spermatogonial differentiation. Inhibition of glucose conversion to glucose-6-phosphate or pentose phosphate pathway also repressed the formation of c-Kit+ differentiating germ cells, suggesting that metabolites produced from glycolysis are required for spermatogonial differentiation. We further demonstrated that the expression levels of several metabolic regulators and enzymes were significantly altered upon RA-induced differentiation, with both RNA-seq and quantitative proteomic analyses. Taken together, our data unveil a critically regulated bioenergetic balance between glycolysis and mitochondrial respiration that is required for spermatogonial proliferation and differentiation.
T-cells produce acidic niches in lymph nodes to suppress their own effector functions
Authors: Wu Hao , Estrella Veronica , Beatty Matthew , Abrahams Dominique , El-Kenawi Asmaa , Russell Shonagh , Ibrahim-Hashim Arig , Longo Dario Livio , Reshetnyak Yana K. , Moshnikova Anna , Andreev Oleg A. , Luddy Kimberly , Damaghi Mehdi , Kodumudi Krithika , Pillai Smitha R. , Enriquez-Navas Pedro , Pilon-Thomas Shari , Swietach Pawel , Gillies Robert J. 
Published: August 2020

AbstractThe acidic pH of tumors profoundly inhibits effector functions of activated CD8 + T-cells. We hypothesize that this is a physiological process in immune regulation, and that it occurs within lymph nodes (LNs), which are likely acidic because of low convective flow and high glucose metabolism. Here we show by in vivo fluorescence and MR imaging, that LN paracortical zones are profoundly acidic. These acidic niches are absent in athymic Nu/Nu and lymphodepleted mice, implicating T-cells in the acidifying process. T-cell glycolysis is inhibited at the low pH observed in LNs. We show that this is due to acid inhibition of monocarboxylate transporters (MCTs), resulting in a negative feedback on glycolytic rate. Importantly, we demonstrate that this acid pH does not hinder initial activation of naïve T-cells by dendritic cells. Thus, we describe an acidic niche within the immune system, and demonstrate its physiological role in regulating T-cell activation.
OSMR controls glioma stem cell respiration and confers resistance of glioblastoma to ionizing radiation
Authors: Sharanek Ahmad , Burban Audrey , Laaper Matthew , Heckel Emilie , Joyal Jean-Sebastien , Soleimani Vahab D. , Jahani-Asl Arezu 
Published: August 2020

AbstractGlioblastoma contains a rare population of self-renewing brain tumor stem cells (BTSCs) which are endowed with properties to proliferate, spur the growth of new tumors, and at the same time, evade ionizing radiation (IR) and chemotherapy. However, the drivers of BTSC resistance to therapy remain unknown. The cytokine receptor for oncostatin M (OSMR) regulates BTSC proliferation and glioblastoma tumorigenesis. Here, we report our discovery of a mitochondrial OSMR that confers resistance to IR via regulation of oxidative phosphorylation, independent of its role in cell proliferation. Mechanistically, OSMR is targeted to the mitochondrial matrix via the presequence translocase-associated motor complex components, mtHSP70 and TIM44. OSMR interacts with NADH ubiquinone oxidoreductase 1/2 (NDUFS1/2) of complex I and promotes mitochondrial respiration. Deletion of OSMR impairs spare respiratory capacity, increases reactive oxygen species, and sensitizes BTSCs to IR-induced cell death. Importantly, suppression of OSMR improves glioblastoma response to IR and prolongs lifespan.
Vulnerability of progeroid smooth muscle cells to biomechanical forces is mediated by MMP13
Authors: Pitrez Patricia R. , Estronca Luís , Monteiro Luís Miguel , Colell Guillem , Vazão Helena , Santinha Deolinda , Harhouri Karim , Thornton Daniel , Navarro Claire , Egesipe Anne-Laure , Carvalho Tânia , Dos Santos Rodrigo L. , Lévy Nicolas , Smith James C. , de Magalhães João Pedro , Ori Alessandro , Bernardo Andreia , De Sandre-Giovannoli Annachiara , Nissan Xavier , Rosell Anna , Ferreira Lino 
Published: August 2020

AbstractHutchinson-Gilford Progeria Syndrome (HGPS) is a premature aging disease in children that leads to early death. Smooth muscle cells (SMCs) are the most affected cells in HGPS individuals, although the reason for such vulnerability remains poorly understood. In this work, we develop a microfluidic chip formed by HGPS-SMCs generated from induced pluripotent stem cells (iPSCs), to study their vulnerability to flow shear stress. HGPS-iPSC SMCs cultured under arterial flow conditions detach from the chip after a few days of culture; this process is mediated by the upregulation of metalloprotease 13 (MMP13). Importantly, double-mutant LmnaG609G/G609GMmp13−/− mice or LmnaG609G/G609GMmp13+/+ mice treated with a MMP inhibitor show lower SMC loss in the aortic arch than controls. MMP13 upregulation appears to be mediated, at least in part, by the upregulation of glycocalyx. Our HGPS-SMCs chip represents a platform for developing treatments for HGPS individuals that may complement previous pre-clinical and clinical treatments.
Lithium niobate photonic-crystal electro-optic modulator
Authors: Li Mingxiao , Ling Jingwei , He Yang , Javid Usman A. , Xue Shixin , Lin Qiang 
Published: August 2020

AbstractModern advanced photonic integrated circuits require dense integration of high-speed electro-optic functional elements on a compact chip that consumes only moderate power. Energy efficiency, operation speed, and device dimension are thus crucial metrics underlying almost all current developments of photonic signal processing units. Recently, thin-film lithium niobate (LN) emerges as a promising platform for photonic integrated circuits. Here, we make an important step towards miniaturizing functional components on this platform, reporting high-speed LN electro-optic modulators, based upon photonic crystal nanobeam resonators. The devices exhibit a significant tuning efficiency up to 1.98 GHz V−1, a broad modulation bandwidth of 17.5 GHz, while with a tiny electro-optic modal volume of only 0.58μm3. The modulators enable efficient electro-optic driving of high-Q photonic cavity modes in both adiabatic and non-adiabatic regimes, and allow us to achieve electro-optic switching at 11 Gb s−1with a bit-switching energy as low as 22 fJ. The demonstration of energy efficient and high-speed electro-optic modulation at the wavelength scale paves a crucial foundation for realizing large-scale LN photonic integrated circuits that are of immense importance for broad applications in data communication, microwave photonics, and quantum photonics.
CTCF-mediated chromatin looping in EGR2 regulation and SUZ12 recruitment critical for peripheral myelination and repair
Authors: Wang Jincheng , Wang Jiajia , Yang Lijun , Zhao Chuntao , Wu Laiman Natalie , Xu Lingli , Zhang Feng , Weng Qinjie , Wegner Michael , Lu Q. Richard 
Published: August 2020

AbstractChromatin organization is critical for cell growth, differentiation, and disease development, however, its functions in peripheral myelination and myelin repair remain elusive. In this report, we demonstrate that the CCCTC-binding factor (CTCF), a crucial chromatin organizer, is essential for Schwann cell myelination and myelin regeneration after nerve injury. Inhibition of CTCF or its deletion blocks Schwann cell differentiation at the pro-myelinating stage, whereas overexpression of CTCF promotes the myelination program. We find that CTCF establishes chromatin interaction loops between enhancer and promoter regulatory elements and promotes expression of a key pro-myelinogenic factor EGR2. In addition, CTCF interacts with SUZ12, a component of polycomb-repressive-complex 2 (PRC2), to repress the transcriptional program associated with negative regulation of Schwann cell maturation. Together, our findings reveal a dual role of CTCF-dependent chromatin organization in promoting myelinogenic programs and recruiting chromatin-repressive complexes to block Schwann cell differentiation inhibitors to control peripheral myelination and repair.
Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints
Authors: Kong Yi Wen , Dreaden Erik C. , Morandell Sandra , Zhou Wen , Dhara Sanjeev S. , Sriram Ganapathy , Lam Fred C. , Patterson Jesse C. , Quadir Mohiuddin , Dinh Anh , Shopsowitz Kevin E. , Varmeh Shohreh , Yilmaz Ömer H. , Lippard Stephen J. , Reinhardt H. Christian , Hemann Michael T. , Hammond Paula T. , Yaffe Michael B. 
Published: August 2020

AbstractIn response to DNA damage, a synthetic lethal relationship exists between the cell cycle checkpoint kinase MK2 and the tumor suppressor p53. Here, we describe the concept of augmented synthetic lethality (ASL): depletion of a third gene product enhances a pre-existing synthetic lethal combination. We show that loss of the DNA repair protein XPA markedly augments the synthetic lethality between MK2 and p53, enhancing anti-tumor responses alone and in combination with cisplatin chemotherapy. Delivery of siRNA-peptide nanoplexes co-targeting MK2 and XPA to pre-existing p53-deficient tumors in a highly aggressive, immunocompetent mouse model of lung adenocarcinoma improves long-term survival and cisplatin response beyond those of the synthetic lethal p53 mutant/MK2 combination alone. These findings establish a mechanism for co-targeting DNA damage-induced cell cycle checkpoints in combination with repair of cisplatin-DNA lesions in vivo using RNAi nanocarriers, and motivate further exploration of ASL as a generalized strategy to improve cancer treatment.