Effect of Zn doping on phase transition and electronic structures of Heusler-type Pd2Cr-based alloys: from normal to all-d-metal Heusler

Based on first-principles calculations, for Heusler alloys Pd₂CrZ (Z = Al, Ga, In, Tl, Si, Sn, P, As, Sb, Bi, Se, Te, Zn), the effect of Zn doping on their phase transition and electronic structure has been studied in this work. These alloys can be divided into two classes: (i) all-d-metal Heusler Pd₂CrZn and (ii) other normal Heusler alloys Pd₂CrZ (Z = Al, Ga, In, Tl, Si, Sn, P, As, Sb, Bi, Se, Te). For all-d-metal Heusler alloy Pd₂CrZn, transition metal element Zn behaves like a main group element due to its full 3d occupied state, and therefore the Zn atoms tend to occupy Wyckoff sites D (0.75, 0.75, 0.75) instead of replacing Pd atoms at A sites (0, 0, 0). The stable tetragonal L1₀ state is obtained via tetragonal deformation and the L1₀ stable state can be tuned by the uniform strain. The stability of the tetragonal state is analyzed and proved via calculation of the density of states (DOSs) and the phonon spectrum. For the series of normal Heusler alloys Pd₂CrZ, doping with Zn atoms can induce or strengthen the martensitic transformation, or regulate the large c/a ratios to a more reasonable range. It is hoped that this work can provide some guidance for further studies of the relationship between all-d-metal and normal Heusler alloys in the future.

By first-principles calculations, for Heusler alloys Pd₂CrZ (Z = Al, Ga, In, Tl, Si, Sn, P, As, Sb, Bi, Se, Te, Zn), the effect of Zn doping on their phase transition and electronic structure has been studied in this work.     

RNA quality control and protein aggregates in amyotrophic lateral sclerosis: A review

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in adults. The biologic basis of ALS remains unknown. However, ALS research has taken a dramatic turn over the past 4 years. Ground breaking discoveries of mutations of genes that encode RNA processing proteins, and demonstration that abnormal aggregates of these and other proteins precede motor neuron loss in familial and sporadic ALS, have initiated a paradigm shift in understanding the pathogenic mechanisms of ALS. Curiously, some of these RNA binding proteins have prion‐like domains, with a propensity to self‐aggregation. The emerging hypothesis that a focal cascade of toxic protein aggregates, and their consequent non–cell‐autonomous spread to neighborhood groups of neurons, fits the classical temporo‐spatial progression of ALS. This article reviews the current research efforts toward understanding the role of RNA‐processing regulation and protein aggregates in ALS. Muscle Nerve 47:330‐338, 2013     

The history of parkinsonism: Descriptions in ancient Indian medical literature

The clinical syndrome of parkinsonism was identified in ancient India even before the period of Christ and was treated methodically. The earliest reference to bradykinesia dates to 600 bc . Evidences prove that as early as 300 bc , Charaka proposed a coherent picture of parkinsonism by describing tremor, rigidity, bradykinesia, and gait disturbances as its components. The scenario was further developed by Madhava, Vagbhata, and Dalhana all through history. The 15th‐century classic “Bhasava rajyam” introduced the term kampavata, which may be regarded as an ayurvedic analogue of parkinsonism. The pathogenesis of kampavata centered on the concept of imbalance in the vata factor, which controls psychomotor activities. The essential element in therapy was the administration of powdered seed of Mucuna pruriens, or atmagupta, which as per reports, contains 4%?6% of levodopa. In addition to proving the existence and identification of parkinsonism in ancient India, the study points to the significance of ancient Indian Sanskrit works in medical history. © 2013 Movement Disorder Society