No abstract

The strain effect on the phase stability of bulk HfO2 is theoretically investigated with the density functional calculations. The origin of the ferroelectric (FE) characteristic in HfO2 is considered to be the formation of a non-centrosymmetric polar orthorhombic (PO) phase. The centrosymmetric nonpolar orthorhombic (O) phase is an antiferroelectric (AFE) structure, which has a smaller energy than PO-phase at unstrained condition. Applied biaxial strain can manipulate the relative stability among phases and also the ferroelectricity. Compressive strain is favored to transform HfO2 from monoclinic to PO-phase. The PO-phase HfO2 possesses the ferroelectricity with the remnant polarization of 66 µC/cm2 and the energy barrier of 70 meV/atom for the polarization switching from up to down. Tensile strain is found out to raise the relative energy of AFE state with respect to FE state. Furthermore, the Al doping in HfO2 could lower the energy barrier for polarization switching and also enhance the population of PO-phase.

No abstract

Introduction Frontal variant of Alzheimer's disease (fvAD) is a rare nonamnestic syndrome of Alzheimer's disease (AD). Differentiating it from behavior variant of frontotemporal dementia (bvFTD), which has implications for treatment responses and prognosis, remains a clinical challenge. Methods Molecular neuroimaging and biofluid markers were performed for the index patient for accurate premortem diagnosis of fvAD. The clinical, neuroimaging, and biofluid characteristics of the patient were compared to those reported in previous studies of fvAD from 1999 to 2019. Results A 66‐year‐old man presented with progressive executive dysfunction, personality and behavioral changes, and memory decline since age 59. He had no family history of neurodegenerative disorders. A stimulus‐sensitive myoclonus was noted over his left upper extremity. Neuropsychological assessment revealed moderate dementia with a Mini‐Mental State Exam score of 10/30 and compromised executive and memory performance. Brain imaging showed asymmetrical atrophy and hypometabolism over the right frontal and temporal areas, mimicking bvFTD. However, we observed increased tau depositions based on 18F‐labeled T807 Tau PET in these areas and diffusely increased amyloid deposition based on 11C‐labeled Pittsburgh compound B positron emission tomography (PET). Plasma biomarker measures indicated an AD profile with increased Aβ1‐42 (18.66 pg/ml; cutoff: 16.42 pg/ml), Aβ1‐42/Aβ1‐40 ratio (0.45; cutoff: 0.30), total tau (29.78 pg/ml; cutoff: 23.89 pg/ml), and phosphorylated tau (4.11 pg/ml; cutoff: 3.08 pg/ml). These results supported a diagnosis of fvAD. Conclusions Our results with asymmetrical presentations extend current knowledge about this rare AD variant. Application of biofluid and molecular imaging markers could assist in early, accurate diagnosis.

In this work, the pathways for polarization switching of hafnium oxide (HfO 2 ) orthorhombic phase were simulated via density functional theory. The energy barriers vary from 30.7 to 69.3 meV/atom depending on the transition states taken in the process of polarization switching. With further analysis, it is found that the pathway via transition state of the Pbcm phase is suitable for the domain-wall motion mechanism for polarization switching but bears the highest energy barrier. On the other hand, the pathways via the tetragonal-like transition state with the lowest energy barrier suggest the uniform switching mechanism. For HfO 2 films composed of different sizes of grains, a uniform switching and domain-wall motion mechanism could be activated in small and large grains.

No abstract

Background: Chromosome 6p25 deletion syndrome is a rare neurocristopathy with variable clinical features. The objective of the current study was to describe a novel phenotype for autosomaldominant chromosome 6p25 deletion syndrome. The presentation included bilateral basal ganglia and subcortical calcifications and juvenile parkinsonism, resembling primary familial brain calcification. Methods: Phenotypic characterization, exome sequencing, and oligonucleotide array were carried out in the index family. Results: The index patient and her mother had a history of developmental delay, mild facial dysmorphism, Axenfield eye anomalies, slight intellectual disability, and subsequently developed levodopa-responsive parkinsonism in early adulthood. Brain-computed tomography showed bilateral basal ganglia and subcortical calcifications. Magnetic resonance imaging revealed diffuse white matter lesions. A 99mTc TRODAT singlephoton emission computed tomography scan revealed bilateral dopaminergic denervation. Whole-exome sequencing and oligonucleotide array-based comparative genomic hybridization revealed a 2.27-Mb chromosome 6pter-p24 deletion, which cosegregated within the family. Conclusions: Our findings extended the current phenotypic spectrum of chromosome 6p25 deletion syndrome.

No abstract