Electronic structure of the Ni-Pd-P and Ni-Pt-P metallic glasses: A pulsed NMR study

A pulsed NMR and magnetic susceptibility study of the electronic structure is reported for the rapidly quenched metallic glass systems: (Ni0.50Pd0.50)100-xPx (where 16≦x≦26.5), (NiyPd1-y)80P20 (where 0.20≦y≦0.80), and (NiyPt1-y)75P25 (where 0.20≦y≦0.68). The 31P Knight shift and nuclear spin-lattice relaxation rate in all three systems depend only on the P concentration, x, and not the Ni concentration, y, nor whether the second transition metal is Pd or Pt. Both the shift and relaxation rate for 31P are attributed solely to the direct contact hyperfine interaction. The 195Pt Knight shift and magnetic susceptibility for (NiyPt1-y)75P25 do depend on both the Ni concentration and temperature, enabling a determination of the contributions to the shift arising from the direct contact hyperfine and core polarization interactions. The results are discussed in terms of a rigid two-band picture with estimates being made for the s- and d-band densities of states and hyperfine coupling constants. There is strong evidence for a transfer of charge from the P metalloid atoms (M) to the d states of the transition-metal atoms (T), which is consistent with the dense random packing model for T100-xMx metallic glasses

Specific binding of TES-23 antibody to tumour vascular endothelium in mice, rats and human cancer tissue: a novel drug carrier for cancer targeting therapy

The tissue distribution of anti-tumour vascular endothelium monoclonal antibody (TES-23) produced by immunizing with plasma membrane vesicles from isolated rat tumour-derived endothelial cells (TECs) was assessed in various tumour-bearing animals. Radiolabelled TES-23 dramatically accumulated in KMT-17 fibrosarcoma, the source of isolated TECs after intravenous injection. In Meth-A fibrosarcoma, Colon-26 adenocarcinoma in BALB/c mice and HT-1080 human tumour tissue in nude mice, radioactivities of 125I-labelled TES-23 were also up to 50 times higher than those of control antibody with little distribution to normal tissues. The selective recognition of TES-23 to TECs was competitively blocked by preadministration of unlabelled TES-23 in vivo. Furthermore, immunostaining of human tissue sections showed specific binding of TES-23 on endothelium in oesophagus cancers. These results indicate that tumour vascular endothelial cells express common antigen in different tumour types of various animal species. In order to clarify the efficacy of TES-23 as a drug carrier, an immunoconjugate, composed of TES-23 and neocarzinostatin, was tested for its anti-tumour effect in rats bearing KMT-17 fibrosarcomas. The immunoconjugate (TES-23-NCS) caused marked regression of the tumour, accompanied by haemorrhagic necrosis. Thus, from a clinical view, TES-23 would be a novel drug carrier because of its high specificity to tumour vascular endothelium and its application to many types of cancer. © 1999 Cancer Research Campaig

Mammalian BTBD12 (SLX4) Protects against Genomic Instability during Mammalian Spermatogenesis

The mammalian ortholog of yeast Slx4, BTBD12, is an ATM substrate that functions as a scaffold for various DNA repair activities. Mutations of human BTBD12 have been reported in a new sub-type of Fanconi anemia patients. Recent studies have implicated the fly and worm orthologs, MUS312 and HIM-18, in the regulation of meiotic crossovers arising from double-strand break (DSB) initiating events and also in genome stability prior to meiosis. Using a Btbd12 mutant mouse, we analyzed the role of BTBD12 in mammalian gametogenesis. BTBD12 localizes to pre-meiotic spermatogonia and to meiotic spermatocytes in wildtype males. Btbd12 mutant mice have less than 15% normal spermatozoa and are subfertile. Loss of BTBD12 during embryogenesis results in impaired primordial germ cell proliferation and increased apoptosis, which reduces the spermatogonial pool in the early postnatal testis. During prophase I, DSBs initiate normally in Btbd12 mutant animals. However, DSB repair is delayed or impeded, resulting in persistent γH2AX and RAD51, and the choice of repair pathway may be altered, resulting in elevated MLH1/MLH3 focus numbers at pachynema. The result is an increase in apoptosis through prophase I and beyond. Unlike yeast Slx4, therefore, BTBD12 appears to function in meiotic prophase I, possibly during the recombination events that lead to the production of crossovers. In line with its expected regulation by ATM kinase, BTBD12 protein is reduced in the testis of Atm−/− males, and Btbd12 mutant mice exhibit increased genomic instability in the form of elevated blood cell micronucleus formation similar to that seen in Atm−/− males. Taken together, these data indicate that BTBD12 functions throughout gametogenesis to maintain genome stability, possibly by co-ordinating repair processes and/or by linking DNA repair events to the cell cycle via ATM

An improved calculation method of inductance and capacitances in ?1 circuits for resonant power amplifiers

In the paper an improved method of calculation of the inductance and capacitances in the ?1 circuit for Class A, AB, B, and C resonant power amplifiers is presented. This method is based on an assumption that the quality factor of the inductor is inite and the capacitors are lossless. The input parameters for calculations are the amplifier load resistance, the transistor load resistance, the quality factor of the inductor, the loaded quality factor of the designed circuit, and the operating frequency. The presented method allows reducing the required regulation range of ?1 circuits elements In built resonant amplifiers as compared to the traditional calculation methods assuming lossless capacitors and inductor. This advantage is important, in particular, for long- and medium-wave transistor power amplifiers, where capacitances in ?1 circuits are high comparing to typical trimming capacitors