The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells.

XRCC4-like factor (XLF), also known as Cernunnos, is a protein encoded by the human NHEJ1 gene and an important repair factor for DNA double-strand breaks. In this study, we have found that XLF is over-expressed in HPV(+) versus HPV(-) head and neck squamous cell carcinoma (HNSCC) and significantly down-regulated in the HNSCC cell lines expressing high level of mutant p53 protein versus those cell lines harboring wild-type TP53 gene with low p53 protein expression. We have also demonstrated that Werner syndrome protein (WRN), a member of the NHEJ repair pathway, binds to both mutant p53 protein and NHEJ1 gene promoter, and siRNA knockdown of WRN leads to the inhibition of XLF expression in the HNSCC cells. Collectively, these findings suggest that WRN and p53 are involved in the regulation of XLF expression and the activity of WRN might be affected by mutant p53 protein in the HNSCC cells with aberrant TP53 gene mutations, due to the interaction of mutant p53 with WRN. As a result, the expression of XLF in these cancer cells is significantly suppressed. Our study also suggests that XLF is over-expressed in HPV(+) HNSCC with low expression of wild type p53, and might serve as a potential biomarker for HPV(+) HNSCC. Further studies are warranted to investigate the mechanisms underlying the interactive role of WRN and XLF in NHEJ repair pathway

Observation of Small Polaron and Acoustic Phonon Coupling in Ultrathin La0.7Sr0.3MnO3/SrTiO3 Structures

Understanding the underlying physics of interactions among various quasi-particles is a fundamental issue for the application of spintronics and photonics. Here the observation of a coupling between the small polarons in the nanoscale ultrathin La0.7Sr0.3MnO3 (LSMO) films and the acoustic phonons in the SrTiO3 (STO) substrate using ultrafast pump–probe spectroscopy has been reported. According to the temperature- and wavelength-dependent measurements, the amplitudes of the acoustic phonons are suppressed by tuning the small polarons absorption. This shows a coupled relationship between the acoustic phonons and the small polarons. At the probe photon energy of 1.55 eV where the polaron absorption is dominant, the acoustic phonons become unobservable. Furthermore, by performing the pump fluence dependent measurements on the LSMO films with different thicknesses, smaller acoustic phonon amplitudes are found in the thinner film with stronger small polaron binding energy. Such a coupled nature can be utilized to manipulate the small polarons using the acoustic phonons or vice versa, which is of great importance in device applications of colossal magnetoresistance materials

Ultrafast Orbital-Oriented Control of Magnetization in Half-Metallic La0.7Sr0.3MnO3 Films

Manipulating spins by ultrafast pulse laser provides a new avenue to switch the magnetization for spintronic applications. While the spin–orbit coupling is known to play a pivotal role in the ultrafast laser-induced demagnetization, the effect of the anisotropic spin–orbit coupling on the transient magnetization remains an open issue. This study uncovers the role of anisotropic spin–orbit coupling in the spin dynamics in a half-metallic La0.7Sr0.3MnO3 film by ultrafast pump–probe technique. The magnetic order is found to be transiently enhanced or attenuated within the initial sub-picosecond when the probe light is tuned to be s- or p-polarized, respectively. The subsequent slow demagnetization amplitude follows the fourfold symmetry of the dx2 y2 orbitals as a function of the polarization angles of the probe light. A model based on the Elliott–Yafet spin-flip scatterings is proposed to reveal that the transient magnetization enhancement is related to the spin-mixed states arising from the anisotropic spin–orbit coupling. The findings provide new insights into the spin dynamics in magnetic systems with anisotropic spin–orbit coupling as well as perspectives for the ultrafast control of information process in spintronic devices

The clinical correlation between Alzheimer's disease and epilepsy

Alzheimer's disease and epilepsy are common nervous system diseases in older adults, and their incidence rates tend to increase with age. Patients with mild cognitive impairment and Alzheimer's disease are more prone to have seizures. In patients older than 65 years, neurodegenerative conditions accounted for ~10% of all late-onset epilepsy cases, most of which are Alzheimer's disease. Epilepsy and seizure can occur in the early and late stages of Alzheimer's disease, leading to functional deterioration and behavioral alterations. Seizures promote amyloid-β and tau deposits, leading to neurodegenerative processes. Thus, there is a bi-directional association between Alzheimer's disease and epilepsy. Epilepsy is a risk factor for Alzheimer's disease and, in turn, Alzheimer's disease is an independent risk factor for developing epilepsy in old age. Many studies have evaluated the shared pathogenesis and clinical relevance of Alzheimer's disease and epilepsy. In this review, we discuss the clinical associations between Alzheimer's disease and epilepsy, including their incidence, clinical features, and electroencephalogram abnormalities. Clinical studies of the two disorders in recent years are summarized, and new antiepileptic drugs used for treating Alzheimer's disease are reviewed

Thermal induced spin-polarized current protected by spin-momentum locking in nanowires

Spin-momentum locking arising from strong spin-orbit coupling is one of the key natures of topological materials. Since charge can induce a spin polarization due to spin-momentum locking, the search for materials that exhibit this feature has become one of the top priorities in the field of spintronics. In this paper, we report the electrical detection of the spin-transport properties of nanowires, using a nonlocal geometry measurement. A clear hysteresis voltage signal, which depends on the relative orientations between the magnetization of the ferromagnetic electrodes and the carrier spin polarization, has been observed. The hysteresis voltage states can be reversed by altering the electron movement direction, providing direct evidence of the spin-momentum locking feature of nanowires and revealing its topological nature. Furthermore, the current-dependent measurement suggests that the charge (spin) current is induced by thermal effect, which utilizes the thermoelectric properties of . Using the thermal effect to control the spin-polarized current protected by spin-momentum locking offers possibilities for small-sized devices based on the topological materials

GJB2 mutation spectrum in 2063 Chinese patients with nonsyndromic hearing impairment

Background: Mutations in GJB2 are the most common molecular defects responsible for autosomal recessive nonsyndromic hearing impairment (NSHI). The mutation spectra of this gene vary among different ethnic groups. Methods: In order to understand the spectrum and frequency of GJB2 mutations in the Chinese population, the coding region of the GJB2 gene from 2063 unrelated patients with NSHI was PCR amplified and sequenced. Results: A total of 23 pathogenic mutations were identified. Among them, five (p.W3X, c.99delT, c.155_c.158delTCTG, c.512_c.513insAACG, and p.Y152X) are novel. Three hundred and seven patients carry two confirmed pathogenic mutations, including 178 homozygotes and 129 compound heterozygotes. One hundred twenty five patients carry only one mutant allele. Thus, GJB2 mutations account for 17.9% of the mutant alleles in 2063 NSHI patients. Overall, 92.6% (684/739) of the pathogenic mutations are frame-shift truncation or nonsense mutations. The four prevalent mutations; c.235delC, c.299_c.300delAT, c.176_c.191del16, and c.35delG, account for 88.0% of all mutantalleles identified. The frequency of GJB2 mutations (alleles) varies from 4% to 30.4% among different regions of China. It also varies among different sub-ethnic groups. Conclusion: In some regions of China, testing of the three most common mutations can identify at least one GJB2 mutant allele in all patients. In other regions such as Tibet, the three most common mutations account for only 16% the GJB2 mutant alleles. Thus, in this region, sequencing of GJB2 would be recommended. In addition, the etiology of more than 80% of the mutant alleles for NSHI in China remains to be identified. Analysis of other NSHI related genes will be necessary

The complete mitochondrial genome sequence and gene organization of Cryodraco antarcticus (Perciformes, Channichthyidae) with phylogenetic consideration

The complete mitochondrial genome DNA sequence of Cryodraco antarcticus was 17,857 bp in size. It consists of 13 protein-coding genes, 2 ribosomal RNAs, 22 transfer RNAs, and one control region. Among 22 tRNA genes, 8 tRNAs were encoded on the L-strand. The overall base composition of the genome is 26.45% for A, 25.96% for T, 29.78% for C, and 17.81% for G. The phylogenetic tree suggested C. antarcticus was genetically closest to some species in family Channichthyidae. This study could provide valuable information for further studies on population structure, conservation genetics and molecular evolution of C. antarcticus

The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells

XRCC4-like factor (XLF), also known as Cernunnos, is a protein encoded by the human NHEJ1 gene and an important repair factor for DNA double-strand breaks. In this study, we have found that XLF is over-expressed in HPV(+) versus HPV(-) head and neck squamous cell carcinoma (HNSCC) and significantly down-regulated in the HNSCC cell lines expressing high level of mutant p53 protein versus those cell lines harboring wild-type TP53 gene with low p53 protein expression. We have also demonstrated that Werner syndrome protein (WRN), a member of the NHEJ repair pathway, binds to both mutant p53 protein and NHEJ1 gene promoter, and siRNA knockdown of WRN leads to the inhibition of XLF expression in the HNSCC cells. Collectively, these findings suggest that WRN and p53 are involved in the regulation of XLF expression and the activity of WRN might be affected by mutant p53 protein in the HNSCC cells with aberrant TP53 gene mutations, due to the interaction of mutant p53 with WRN. As a result, the expression of XLF in these cancer cells is significantly suppressed. Our study also suggests that XLF is over-expressed in HPV(+) HNSCC with low expression of wild type p53, and might serve as a potential biomarker for HPV(+) HNSCC. Further studies are warranted to investigate the mechanisms underlying the interactive role of WRN and XLF in NHEJ repair pathway