Magnetic Properties of Pr0.7Ca0.3MnO3/SrRuO3 Superlattices

High-quality Pr0.7Ca0.3MnO3/SrRuO3 superlattices were fabricated by pulsed laser deposition and were investigated by high-resolution transmission electron microscopy and SQUID magnetometry. Superlattices with orthorhombic and tetragonal SrRuO3 layers were investigated. The superlattices grew coherently; in the growth direction Pr0.7Ca0.3MnO3 layers were terminated by MnO2- and SrRuO3 layers by RuO2-planes. All superlattices showed antiferromagnetic interlayer coupling in low magnetic fields. The coupling strength was significantly higher for orthorhombic than for tetragonal symmetry of the SrRuO3 layers. The strong interlayer exchange coupling in the superlattice with orthorhombic SrRuO3 layers led to a magnetization reversal mechanism with a partially inverted hysteresis loop.Comment: 12 pages, 4 figure

Orthorhombic to tetragonal transition of SrRuO3 layers in Pr0.7Ca0.3MnO3/SrRuO3 superlattices

High-quality Pr0.7Ca0.3MnO3/SrRuO3 superlattices with ultrathin layers were fabricated by pulsed laser deposition on SrTiO3 substrates. The superlattices were studied by atomically resolved scanning transmission electron microscopy, high-resolution transmission electron microscopy, resistivity and magnetoresistance measurements. The superlattices grew coherently without growth defects. Viewed along the growth direction, SrRuO3 and Pr0.7Ca0.3MnO3 layers were terminated by RuO2 and MnO2, respectively, which imposes a unique structure to their interfaces. Superlattices with a constant thickness of the SrRuO3 layers, but varying thickness of the Pr0.7Ca0.3MnO3 layers showed a change of crystalline symmetry of the SrRuO3 layers. At a low Pr0.7Ca0.3MnO3 layer thickness of 1.5 nm transmission electron microscopy proved the SrRuO3 layers to be orthorhombic, whereas these were non-orthorhombic for a Pr0.7Ca0.3MnO3 layer thickness of 4.0 nm. Angular magnetoresistance measurements showed orthorhombic (with small monoclinic distortion) symmetry in the first case and tetragonal symmetry of the SrRuO3 layers in the second case. Mechanisms driving this orthorhombic to tetragonal transition are briefly discussed.Comment: 23 pages, 12 figure

On the electronic properties of a single dislocation

A detailed knowledge of the electronic properties of individual dislocations is necessary for next generation nanodevices. Dislocations are fundamental crystal defects controlling the growth of different nanostructures (nanowires) or appear during device processing. We present a method to record electric properties of single dislocations in thin silicon layers. Results of measurements on single screw dislocations are shown for the first time. Assuming a cross-section area of the dislocation core of about 1 nm2, the current density through a single dislocation is J = 3.8 × 1012 A/cm2 corresponding to a resistivity of ρ ≅ 1 × 10-8 Ω cm. This is about eight orders of magnitude lower than the surrounding silicon matrix. The reason of the supermetallic behavior is the high strain in the cores of the dissociated dislocations modifying the local band structure resulting in high conductive carrier channels along defect cores

Single-electron transitions in one-dimensional native nanostructures

Low-temperature measurements proved the existence of a two-dimensional electron gas at defined dislocation arrays in silicon. As a consequence, single-electron transitions (Coulomb blockades) are observed. It is shown that the high strain at dislocation cores modifies the band structure and results in the formation of quantum wells along dislocation lines. This causes quantization of energy levels inducing the formation of Coulomb blockades

Crystal structure of cleaved vaspin (serpinA12)

The adipokine vaspin (serpinA12) is mainly expressed in white adipose tissue and exhibits various beneficial effects on obesity-related processes. Kallikrein 7 is the only known target protease of vaspin and is inhibited by the classical serpin inhibitory mechanism involving a cleavage of the reactive center loop between P1 (M378) and P1′ (E379). Here, we present the X-ray structure of vaspin, cleaved between M378 and E379. We provide a comprehensive analysis of differences between the uncleaved and cleaved forms in the shutter, breach, and hinge regions with relation to common molecular features underlying the serpin inhibitory mode. Furthermore, we point out differences towards other serpins and provide novel data underlining the remarkable stability of vaspin. We speculate that the previously reported FKGx1Wx2x3 motif in the breach region may play a decisive role in determining the reactive center loop configuration in the native vaspin state and might contribute to the high thermostability of vaspin. Thus, this structure may provide a basis for future mutational studies

Evolution of the interface structure of bonded Si wafers after high temperature annealing

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X-Ray Co-Crystal Structure Guides the Way to Subnanomolar Competitive Ecto-5 '-Nucleotidase (CD73) Inhibitors for Cancer Immunotherapy

Ecto-5'-nucleotidase (CD73, EC 3.1.3.5) catalyzes the extracellular hydrolysis of AMP yielding adenosine, which induces immunosuppression, angiogenesis, metastasis, and proliferation of cancer cells. CD73 inhibition is therefore proposed as a novel strategy for cancer (immuno)therapy, and CD73 antibodies are currently undergoing clinical trials. Despite considerable efforts, the development of small molecule CD73 inhibitors has met with limited success. To develop a suitable drug candidate, a high resolution (2.05 degrees A) co-crystal structure of the CD73 inhibitor PSB-12379, a nucleotide analogue, in complex with human CD73 is determined. This allows the rational design and development of a novel inhibitor (PSB-12489) with subnanomolar inhibitory potency toward human and rat CD73, high selectivity, as well as high metabolic stability. A co-crystal structure of PSB-12489 with CD73 (1.85 degrees A) reveals the interactions responsible for increased potency. PSB-12489 is the most potent CD73 inhibitor to date representing a powerful tool compound and novel lead structure

Molecular mechanisms of vaspin action: from adipose tissue to skin and bone, from blood vessels to the brain

Visceral adipose tissue derived serine protease inhibitor (vaspin) or SERPINA12 according to the serpin nomenclature was identified together with other genes and gene products that  were specifically expressed or overexpressed in the intra abdominal or visceral adipose tissue  (AT) of the Otsuka Long-Evans Tokushima fatty rat. These rats spontaneously develop visceral  obesity, insulin resistance, hyperinsulinemia and ‐glycemia, as well as hypertension and thus represent a well suited animal model of obesity and related metabolic disorders such as type  2 diabetes.  The follow-up study reporting the cloning, expression and functional characterization of  vaspin suggested the great and promising potential of this molecule to counteract obesity induced insulin resistance and inflammation and has since initiated over 300 publications, clinical and experimental, that have contributed to uncover the multifaceted functions and molecular mechanisms of vaspin action not only in the adipose, but in many different cells, tissues and organs. This review will give an update on mechanistic and structural aspects of vaspin with a focus on its serpin function, the physiology and regulation of vaspin expression, and will summarize the latest on vaspin function in various tissues such as the different adipose tissue depots as well as the vasculature, skin, bone and the brain