Improvement of endurance and switching speed in Hf1-xZrxO2thin films using a nanolaminate structure.

To improve the endurance and polarization switching speed of Hf1-xZrxO2(HZO) ferroelectric films, we designed a 10 nm Hf0.5Zr0.5O2 + ZrO2(HZZ) nanolaminate structure. Three films with different ZrO2interlayers thicknesses were compared to find the optimal condition to implement the effect of the topological domain wall which was proposed recently. The HZZ film were deposited by repeatedly stacking ten HZO (∼0.92 nm) and six ZrO2(∼0.53 nm) layers; they exhibited a dramatic reduction of coercive field without an effective loss of remnant polarization. The endurance at operation voltage increased by more than 100 times compared with that of the solid solution HZO film, and the switching speed was increased by more than two times. The formation of the tetragonal phase-like spacer between the ferroelectric polar regions appears to be the main factor associated with the reduction of the switching barrier and leads to the acceleration of the switching propagation over multiple domains.

Effects of high pressure oxygen annealing on Hf0.5Zr0.5O2ferroelectric device.

We report a high-pressure oxygen annealing (HPOA) process to improve the performance of TiN/Hf0.5Zr0.5O2(HZO)/TiN devices by controlling the number of oxygen vacancies and carbon contaminants. The ferroelectric properties of HZO film after HPOA at 250 °C for 30 min under different oxygen pressures from 0 to 80 bar were evaluated by electrical and structural characterizations. We found that a sample treated with an oxygen pressure at 40 bar exhibited large switchable polarization (2Pr) of approximately 38 and 47µC cm-2in its pristine and wake-up states, respectively. Compared to a control sample, an approximately 40% reduction in the wake-up effect was achieved after HPOA at 40 bar. Improved ferroelectric properties of HZO film can be explained by the appropriate amount of oxygen vacancies and reduced carbon contaminants after HPOA.

High polarization and wake-up free ferroelectric characteristics in ultrathin Hf0.5Zr0.5O2devices by control of oxygen-deficient layer.

The formation of an interfacial layer is believed to affect the ferroelectric properties in HfO2based ferroelectric devices. The atomic layer deposited devices continue suffering from a poor bottom interfacial condition, since the formation of bottom interface is severely affected by atomic layer deposition and annealing process. Herein, the formation of bottom interfacial layer was controlled through deposition of different bottom electrodes (BE) in device structure W/HZO/BE. The transmission electron microscopy (TEM) and x-ray photoelectron spectroscopy analyses done on devices W/HZO/W and W/HZO/IrOxsuggest the strong effect of IrOxin controlling bottom interfacial layer formation while W/HZO/W badly suffers from interfacial layer formation. W/HZO/IrOxdevices show high remnant polarization (2Pr) âˆ¼ 53µC cm-2, wake-up free endurance cycling characteristics, low leakage current with demonstration of low annealing temperature requirement as low as 350 °C, valuable for back-end-of-line integration. Further, sub-5 nm HZO thicknesses-based W/HZO/IrOxdevices demonstrate high 2Prand wake-up free ferroelectric characteristics, which can be promising for low power and high-density memory applications. 2.2 nm, 3 nm, and 4 nm HZO based W/HZO/IrOxdevices show 2Prvalues 13.54, 22.4, 38.23µC cm-2at 4 MV cm-1and 19.96, 30.17, 48.34µC cm-2at 5 MV cm-1, respectively, with demonstration of wake-up free ferroelectric characteristics.

Limb-girdle myasthenia with tubular aggregates associated with novel GFPT1 mutations.

INTRODUCTION: Limb-girdle myasthenia with tubular aggregates (LGM with TAs) is a subtype of congenital myasthenic syndrome caused by recessive mutations of glutamine-fructose-6-phosphate transaminase 1 (GFPT1). METHODS: Clinical and neurophysiological assessment was made in a Korean boy who had proximal limb muscle weakness. Findings suggested a diagnosis of congenital myasthenic syndrome. RESULTS: Muscle biopsy disclosed numerous TAs in muscle fibers, and DNA sequence analysis disclosed 2 novel missense mutations (p.E256Q and p.M499T) in GFPT1. Treatment with oral cholinesterase inhibitors produced a dramatic improvement in muscle strength. CONCLUSIONS: GFPT1 is the key enzyme in the hexosamine biosynthesis pathway, and mutations in GFPT1 cause defective glycosylation in the proteins of the neuromuscular junction. Identification of LGM with TAs among patients with congenital myasthenic syndrome is important because treatment with cholinesterase inhibitors can produce symptomatic improvement.

Homozygous MAPT R406W mutation causing FTDP phenotype: A unique instance of a unique mutation.

Frontotemporal dementia is a neurodegenerative disorder among adults. An autosomal-dominantly form of frontotemporal dementia and parkinsonism linked to chromosome 17q21.2 (FTDP-17) was defined in 1996. The MAPT gene is responsible for the major cases of FTDP-17, and tau also has a role in Alzheimer's disease. So far, different FTDP-17 causing mutations have been identified in the MAPT gene. Among different MAPT mutations, the R406W mutation has been reported with a phenotype resembling Alzheimer's disease. Nonetheless, in this study we have identified the first homozygous case of R406W mutation in an Iranian family which shows characteristics of FTDP, just like the other heterozygous mutations of MAPT. This study clearly indicates that homozygous R406W mutation could result in FTDP phenotype. Our family confirms heterogeneity in the clinical phenotype of MAPT mutations; moreover, in the R406W mutation, a dosage effect is likely to contribute to this clinical heterogeneity.

Mutation analysis of SPAST, ATL1, and REEP1 in Korean Patients with Hereditary Spastic Paraplegia.

BACKGROUND AND PURPOSE: Hereditary spastic paraplegia (HSP) is a genetically heterogeneous group of neurodegenerative disorders that are characterized by progressive spasticity and weakness of the lower limbs. Mutations in the spastin gene (SPAST) are the most common causes of HSP, accounting for 40-67% of autosomal dominant HSP (AD-HSP) and 12-18% of sporadic cases. Mutations in the atlastin-1 gene (ATL1) and receptor expression-enhancing protein 1 gene (REEP1) are the second and third most common causes of AD-HSP, respectively. METHODS: Direct sequence analysis was used to screen mutations in SPAST, ATL1, and REEP1 in 27 unrelated Korean patients with pure and complicated HSP. Multiplex ligation-dependent probe amplification was also performed to detect copy-number variations of the three genes. RESULTS: Ten different SPAST mutations were identified in 11 probands, of which the following 6 were novel: c.760A>T, c.131C>A, c.1351_1353delAGA, c.376_377dupTA, c.1114A>G, and c.1372A>C. Most patients with SPAST mutations had AD-HSP (10/11, 91%), and the frequency of SPAST mutations accounted for 66.7% (10/15) of the AD-HSP patients. No significant correlation was found between the presence of the SPAST mutation and any of the various clinical parameters of pure HSP. No ATL1 and REEP1 mutations were detected. CONCLUSIONS: We conclude that SPAST mutations are responsible for most Korean cases of genetically confirmed AD-HSP. Our observation of the absence of ATL1 and REEP1 mutations needs to be confirmed in larger series.