An extreme magnetoresistance (XMR) has recently been observed in several nonmagnetic semimetals. Increasing experimental and theoretical evidence indicates that the XMR can be driven by either ...topological protection or electron-hole compensation. Here, by investigating the electronic structure of a XMR material, YSb, we present spectroscopic evidence for a special case which lacks topological protection and perfect electron-hole compensation. Further investigations reveal that a cooperative action of a substantial difference between electron and hole mobility and a moderate carrier compensation might contribute to the XMR in YSb.
The dynamics of an order parameter's amplitude and phase determines the collective behaviour of novel states emerging in complex materials. Time- and momentum-resolved pump-probe spectroscopy, by ...virtue of measuring material properties at atomic and electronic time scales out of equilibrium, can decouple entangled degrees of freedom by visualizing their corresponding dynamics in the time domain. Here we combine time-resolved femotosecond optical and resonant X-ray diffraction measurements on charge ordered La(1.75)Sr(0.25)NiO(4) to reveal unforeseen photoinduced phase fluctuations of the charge order parameter. Such fluctuations preserve long-range order without creating topological defects, distinct from thermal phase fluctuations near the critical temperature in equilibrium. Importantly, relaxation of the phase fluctuations is found to be an order of magnitude slower than that of the order parameter's amplitude fluctuations, and thus limits charge order recovery. This new aspect of phase fluctuations provides a more holistic view of the phase's importance in ordering phenomena of quantum matter.
ABSTRACT
Organic acids play a pivotal role in improving plant response to long‐term drought stress. External application of organic acids has been reported to improve drought resistance in several ...species. However, whether organic acids have similar effects in tobacco remains unknown. A screening study of the protective function of organic acids in tobacco and understanding the underlying molecular mechanism would be useful in developing a strategy for drought tolerance.
Several physiological and molecular adaptations to drought including abscisic acid, stomatal closure, reactive oxygen species homeostasis, amino acid accumulation, and drought‐responsive gene expression were observed by exogenous citric acid in tobacco plants.
Exogenous application of 50 mm citric acid to tobacco plants resulted in higher chlorophyll content, net photosynthesis, relative water content, abscisic acid content and lower stomatal conductance, transpiration and water loss under drought conditions. Moreover, reactive oxygen species homeostasis was better maintained through increasing activity of antioxidant enzymes and decreasing hydrogen peroxide content after citric acid pretreatment under drought. Amino acids involved in the TCA cycle accumulated after external application of citric acid under drought stress. Furthermore, several drought stress‐responsive genes also dramatically changed after application of citric acid.
These data support the idea that external application of citric acid enhances drought resistance by affecting physiological and molecular regulation in tobacco. This study provides clear insights into mechanistic details of regulation of amino acid and stress‐responsive gene expression by citric acid in tobacco in response to drought, which is promising for minimizing growth inhibition in agricultural fields.
Exogenous citric acid enhances drought tolerance of tobacco by regulating the amino acid metabolism and stress‐related genes expression.
An array of eight long Ti-6Al-4V rods (diameter: 12 mm; height: 300 mm) have been additively manufactured, vertically and perpendicular to the powder bed, by selective electron beam melting (SEBM). ...The purpose was to identify and understand the challenges of fabricating Ti-6Al-4V samples or parts from a deep powder bed (more than 200-mm deep) by SEBM and the necessity of applying post heat treatment. The resulting microstructure and mechanical properties of these Ti-6Al-4V rods were characterized along their building (
i.e.,
axial) direction by dividing each rod into three segments (top, middle, and bottom), both before (
i.e.,
as-built) and after hot isostatic pressing (HIP). The as-built microstructure of each rod was inhomogeneous; it was coarsest in the top segment, which showed a near equilibrium
α
-
β
lamellar structure, and finest in the bottom segment, which featured a non-equilibrium mixed structure. The tensile properties varied along the rod axis, especially the ductility, but all tensile properties met the requirements specified by ASTM F3001-14. HIP increased the relative density from 99.03 pct of the theoretical density (TD) to 99.90 pct TD and homogenized the microstructure thereby leading to highly consistent tensile properties along the rod axis. The temperature of the stainless steel substrate used in the powder bed was monitored. The as-built inhomogeneous microstructure is attributed to the temperature gradient in the deep powder bed. Post heat treatment is thus necessary for Ti-6Al-4V samples or parts manufactured from a deep powder bed by SEBM. This differs from the additive manufacturing of small samples or parts from a shallow powder bed (less than 100-mm deep) by SEBM.
Aims/hypothesis
FTO
harbours the strongest known obesity-susceptibility locus in Europeans. While there is growing evidence for a role for
FTO
in obesity risk in Asians, its association with type 2 ...diabetes, independently of BMI, remains inconsistent. To test whether there is an association of the
FTO
locus with obesity and type 2 diabetes, we conducted a meta-analysis of 32 populations including 96,551 East and South Asians.
Methods
All studies published on the association between
FTO
-rs9939609 (or proxy
r
2
> 0.98) and BMI, obesity or type 2 diabetes in East or South Asians were invited. Each study group analysed their data according to a standardised analysis plan. Association with type 2 diabetes was also adjusted for BMI. Random-effects meta-analyses were performed to pool all effect sizes.
Results
The
FTO
-rs9939609 minor allele increased risk of obesity by 1.25-fold/allele (
p
= 9.0 × 10
−19
), overweight by 1.13-fold/allele (
p
= 1.0 × 10
−11
) and type 2 diabetes by 1.15-fold/allele (
p
= 5.5 × 10
−8
). The association with type 2 diabetes was attenuated after adjustment for BMI (OR 1.10-fold/allele,
p
= 6.6 × 10
−5
). The
FTO
-rs9939609 minor allele increased BMI by 0.26 kg/m
2
per allele (
p
= 2.8 × 10
−17
), WHR by 0.003/allele (
p
= 1.2 × 10
−6
), and body fat percentage by 0.31%/allele (
p
= 0.0005). Associations were similar using dominant models. While the minor allele is less common in East Asians (12–20%) than South Asians (30–33%), the effect of
FTO
variation on obesity-related traits and type 2 diabetes was similar in the two populations.
Conclusions/interpretation
FTO
is associated with increased risk of obesity and type 2 diabetes, with effect sizes similar in East and South Asians and similar to those observed in Europeans. Furthermore,
FTO
is also associated with type 2 diabetes independently of BMI.
Human neural progenitors from a variety of sources present new opportunities to model aspects of human neuropsychiatric disease in vitro. Such in vitro models provide the advantages of a human ...genetic background combined with rapid and easy manipulation, making them highly useful adjuncts to animal models. Here, we examined whether a human neuronal culture system could be utilized to assess the transcriptional program involved in human neural differentiation and to model some of the molecular features of a neurodevelopmental disorder, such as autism. Primary normal human neuronal progenitors (NHNPs) were differentiated into a post-mitotic neuronal state through addition of specific growth factors and whole-genome gene expression was examined throughout a time course of neuronal differentiation. After 4 weeks of differentiation, a significant number of genes associated with autism spectrum disorders (ASDs) are either induced or repressed. This includes the ASD susceptibility gene neurexin 1, which showed a distinct pattern from neurexin 3 in vitro, and which we validated in vivo in fetal human brain. Using weighted gene co-expression network analysis, we visualized the network structure of transcriptional regulation, demonstrating via this unbiased analysis that a significant number of ASD candidate genes are coordinately regulated during the differentiation process. As NHNPs are genetically tractable and manipulable, they can be used to study both the effects of mutations in multiple ASD candidate genes on neuronal differentiation and gene expression in combination with the effects of potential therapeutic molecules. These data also provide a step towards better understanding of the signaling pathways disrupted in ASD.
Essentials
ARHGEF10 single‐nucleotide polymorphism provides risk of ischemic and atherothrombotic stroke.
The role of ARHGEF10 in platelet function was examined using ARHGEF10 knockout mice.
ARHGEF10 ...deficiency inhibits platelet function and arterial thrombus formation.
ARHGEF10 knockout protects mice from stroke‐induced infarction.
Summary
Background
ARHGEF10, a member of the Rho guanine nucleotide exchange factor (GEF) family, stimulates Rho GTPases. Rho GTPases have been reported to regulate a variety of cellular behaviors, such as cell polarity, cytoskeletal organization, and gene transcription. ARHGEF10 single‐nucleotide polymorphisms are linked to the risk of ischemic stroke. However, the role of ARHGEF10 in platelet function remains unknown.
Objective
To examine the role of ARHGEF10 in platelet function.
Methods
ARHGEF10−/−were generated. We examined the in vitro and in vivo effects of ARHGEF10 knockout on platelet function and arterial thrombosis formation.
Results
ARHGEF10−/− mice had normal platelet counts, but showed altered aggregation in response to thrombin, collagen, ADP, protease‐activated receptor‐4 peptide, and U46619 stimulation. ARHGEF10 knockout influenced platelet spreading on fibrinogen‐coated surfaces, and caused the platelets to show less lamellipodia‐like extension than wild‐type platelets. ARHGEF10 knockout also inhibited platelet clot retraction induced by thrombin stimulation. ARHGEF10 knockout resulted in prolonged tail bleeding time and inhibited the stable thrombus formation induced by FeCl3 in the carotid artery.
Conclusions
ARHGEF10 serves as an important regulator in platelet shape change, spreading, and aggregation. Moreover, ARHGEF10 also plays an important role in arterial thrombosis formation.
Glioblastoma is the most common primary malignant brain tumor of adults and one of the most lethal of all cancers. Patients with this disease have a median survival of 15 months from the time of ...diagnosis despite surgery, radiation, and chemotherapy. New treatment approaches are needed. Recent works suggest that glioblastoma patients may benefit from molecularly targeted therapies. Here, we address the compelling need for identification of new molecular targets. Leveraging global gene expression data from two independent sets of clinical tumor samples (n = 55 and n = 65), we identify a gene coexpression module in glioblastoma that is also present in breast cancer and significantly overlaps with the "metasignature" for undifferentiated cancer. Studies in an isogenic model system demonstrate that this module is downstream of the mutant epidermal growth factor receptor, EGFRvIII, and that it can be inhibited by the epidermal growth factor receptor tyrosine kinase inhibitor Erlotinib. We identify ASPM (abnormal spindle-like microcephaly associated) as a key gene within this module and demonstrate its overexpression in glioblastoma relative to normal brain (or body tissues). Finally, we show that ASPM inhibition by siRNA-mediated knockdown inhibits tumor cell proliferation and neural stem cell proliferation, supporting ASPM as a potential molecular target in glioblastoma. Our weighted gene coexpression network analysis provides a blueprint for leveraging genomic data to identify key control networks and molecular targets for glioblastoma, and the principle eluted from our work can be applied to other cancers.
The oligodendrocyte lineage genes
Olig1 and
Olig2 encode related bHLH proteins that are coexpressed in neural progenitors. Targeted disruption of these two genes sheds light on the ontogeny of ...oligodendroglia and genetic requirements for their development from multipotent CNS progenitors.
Olig2 is required for oligodendrocyte and motor neuron specification in the spinal cord.
Olig1 has roles in development and maturation of oligodendrocytes, evident especially within the brain. Both
Olig genes contribute to neural pattern formation. Neither
Olig gene is required for astrocytes. These findings, together with fate mapping analysis of
Olig-expressing cells, indicate that oligodendrocytes are derived from
Olig-specified progenitors that give rise also to neurons.
We report findings of strong anomalies in both mutual inductance and inelastic Raman spectroscopy measurements of single-unit-cell FeSe film grown on Nb-doped SrTiO3, which occur near the temperature ...where the superconductinglike energy gap opens. Analysis suggests that the anomaly is associated with a broadened ferroelectric transition in a thin layer near the FeSe/SrTiO3 interface. The coincidence of the ferroelectric transition and gap-opening temperatures adds credence to the central role played by the film-substrate interaction on the strong Cooper pairing in this system. We discuss scenarios that could explain such a coincidence.
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