Magnetic Properties of Gadolinium-Doped ZnO Films and Nanostructures

The magnetic properties of Gd-doped ZnO films and nanostructures are important to the development of next-generation spintronic devices. Here, we elucidate the significant role played by Gd-oxygen-deficiency defects in mediating/inducing ferromagnetic coupling in in situ Gd-doped ZnO thin films deposited at low oxygen pressure by pulsed laser deposition (PLD). Samples deposited at higher oxygen pressures exhibited diamagnetic responses. Vacuum annealing was used on these diamagnetic samples (grown at a relatively high oxygen pressures) to create oxygen-deficiency defects with the aim of demonstrating reproducibility of room-temperature ferromagnetism (RTFM). Samples annealed at oxygen environment exhibited superparamagnetism and blocking-temperature effects. The samples possessed secondary phases; Gd segregation led to superparamagnetism. Theoretical studies showed a shift of the 4f level of Gd to the conduction band minimum (CBM) in Gd-doped ZnO nanowires, which led to an overlap with the Fermi level, resulting in strong exchange coupling and consequently RTFM

Multilayer Ferromagnetic Spintronic Devices for Neuromorphic Computing Applications

Spintronics has gone through substantial progress due to its applications in energy-efficient memory, logic and unconventional computing paradigms. Multilayer ferromagnetic thin films are extensively studied for understanding the domain wall and skyrmion dynamics. However, most of these studies are confined to the materials and domain wall/skyrmion physics. In this paper, we present the experimental and micromagnetic realization of a multilayer ferromagnetic spintronic device for neuromorphic computing applications. The device exhibits multilevel resistance states and the number of resistance states increases with lowering temperature. This is supported by the multilevel magnetization behavior observed in the micromagnetic simulations. Furthermore, the evolution of resistance states with spin-orbit torque is also explored in experiments and simulations. Using the multi-level resistance states of the device, we propose its applications as a synaptic device in hardware neural networks and study the linearity performance of the synaptic devices. The neural network based on these devices is trained and tested on the MNIST dataset using a supervised learning algorithm. The devices at the chip level achieve 90\% accuracy. Thus, proving its applications in neuromorphic computing. Furthermore, we lastly discuss the possible application of the device in cryogenic memory electronics for quantum computers

Phosphorylation of cell cycle and apoptosis regulatory protein-1 by stress activated protein kinase P38γ is a novel mechanism of apoptosis signaling by genotoxic chemotherapy

CARP-1, a perinuclear phospho-protein, regulates cell survival and apoptosis signaling induced by genotoxic drugs. However, kinase(s) phosphorylating CARP-1 and down-stream signal transduction events remain unclear. Here we find that CARP-1 Serine (S)626 and Threonine (T)627 substitution to Alanines (AA) inhibits genotoxic drug-induced apoptosis. CARP-1 T627 is followed by a Proline (P), and this TP motif is conserved in vertebrates. Based on these findings, we generated affinity-purified, anti-phospho-CARP-1 T627 rabbit polyclonal antibodies, and utilized them to elucidate chemotherapy-activated, CARP-1-dependent cell growth signaling mechanisms. Our kinase profiling studies revealed that MAPKs/SAPKs phosphorylated CARP-1 T627. We then UV cross-linked protein extracts from Adriamycin-treated HeLa cervical cancer cells with a CARP-1 (614–638) peptide, and conducted liquid chromatography-tandem mass spectrometry (LC-MS/MS) analyses of the peptide-bound protein complexes. This experiment revealed SAPK p38γ interaction with CARP-1 (614–638) peptide. Our studies further established that SAPK p38γ, but not other MAPKs, phosphorylates CARP-1 T627 in cancer cells treated with genotoxic drugs. Loss of p38γ abrogates CARP-1 T627 phosphorylation, and results in enhanced survival of breast cancer cells by genotoxic drugs. CARP-1 T627 phosphorylation was also noted in breast tumors from patients treated with radiation or endocrine therapies. We conclude that genotoxic drugs activate p38γ-dependent CARP-1 T627 phosphorylation to inhibit cell growth