341 research outputs found
Current-driven microwave oscillations in current perpendicular-to-plane spin-valve nanopillars
We study the current and temperature dependences of the microwave voltage
emission of spin-valve nanopillars subjected to an in-plane magnetic field and
a perpendicular-to-plane current. Despite the complex multilayer geometry,
clear microwave emission is shown to be possible and spectral lines as narrow
as 3.8 MHz (at 150 K) are observed.Comment: To appear in Applied Physics Letter
Structure and regulation of mammalian S-adenosylmethionine decarboxylase
In order to understand the structure and regulation of S-adenosylmethionine decarboxylase, cDNA clones encoding this enzyme have been isolated from rat prostate and human fibroblast cDNA libraries. The authenticity of the cDNAs was verified by: (a) transfecting the Chinese hamster ovary cells with the human cDNA in the pcD vector which resulted in a transient 10-20-fold increase in S-adenosylmethionine decarboxylase activity in recipient cells; and (b) translating the mRNA formed by transcription of the cDNA insert in a reticulocyte lysate and recording an increase in S-adenosylmethionine decarboxylase activity. The amino acid sequences deduced from the cDNAs indicate that the human proenzyme for this protein contains 334 amino acids and has a molecular weight of 38,331 whereas the rat proenzyme contains 333 amino acid residues. The human and rat enzymes are very similar having only 11 amino acid differences and the cDNAs are also closely related showing over 90% homology in the 1617-nucleotide overlap which was sequenced. A further indication of the highly conserved nature of mammalian S-adenosylmethionine decarboxylases is that the amino acid sequences deduced from the human and the rat cDNAs contained peptide sequences identical to those previously reported for the purified bovine enzyme. In vitro transcription/translation experiments showed that the proenzyme is converted to two polypeptides of molecular weights about 32,000 and 6,000 in a processing reaction which generates the prosthetic pyruvate group and that the final enzyme contains both polypeptides. Two forms of S-adenosylmethionine decarboxylase mRNA (2.1 and about 3.4-3.6 kilobases) are present in human and rodent tissues and may originate from the utilization of two different polyadenylation signals. Southern blots of rat genomic DNA indicated that the S-adenosylmethionine decarboxylase gene belongs to a multigene family. Depletion of cellular polyamines by inhibitors or ornithine decarboxylase or the aminopropyltransferases led to an increase in the content of S-adenosylmethionine decarboxylase protein and mRNA, but the elevation in the mRNA was not sufficient to account for all of the change in the enzyme level, particularly in cells in which spermine was depleted
Measuring a population of spin waves from the electrical noise of an inductively coupled antenna
We study how a population of spin waves can be characterized from the
analysis of the electrical microwave noise delivered by an inductive antenna
placed in its vicinity. The measurements are conducted on a synthetic
antiferromagnetic thin stripe covered by a micron-sized antenna that feeds a
spectrum analyser after amplification. The antenna noise contains two
contributions. The population of incoherent spin waves generates a fluctuating
field that is sensed by the antenna: this is the "magnon noise". The antenna
noise also contains the contribution of the electronic fluctuations: the
Johnson-Nyquist noise. The latter depends on all impedances within the
measurement circuit; this includes the antenna self-inductance. As a result,
the electronic noise contains information about the magnetic susceptibility,
though it does not inform on the absolute amplitude of the magnetic
fluctuations. For micrometer-sized systems at thermal equilibrium, the
electronic noise dominates and the pure magnon noise cannot be determined. If
in contrast the spinwave bath is not at thermal equilibrium with the
measurement circuit, and if the spinwave population can be changed then one
could measure a mode-resolved effective magnon temperature provided specific
precautions are implemented
Jinx, an MCMV susceptibility phenotype caused by disruption of Unc13d: a mouse model of type 3 familial hemophagocytic lymphohistiocytosis
Mouse cytomegalovirus (MCMV) susceptibility often results from defects of natural killer (NK) cell function. Here we describe Jinx, an N-ethyl-N-nitrosourea–induced MCMV susceptibility mutation that permits unchecked proliferation of the virus, causing death. In Jinx homozygotes, activated NK cells and cytotoxic T lymphocytes (CTLs) fail to degranulate, although they retain the ability to produce cytokines, and cytokine levels are markedly elevated in the blood of infected mutant mice. Jinx was mapped to mouse chromosome 11 on a total of 246 meioses and confined to a 4.60–million basepair critical region encompassing 122 annotated genes. The phenotype was ascribed to the creation of a novel donor splice site in Unc13d, the mouse orthologue of human MUNC13-4, in which mutations cause type 3 familial hemophagocytic lymphohistiocytosis (FHL3), a fatal disease marked by massive hepatosplenomegaly, anemia, and thrombocytopenia. Jinx mice do not spontaneously develop clinical features of hemophagocytic lymphohistiocytosis (HLH), but do so when infected with lymphocytic choriomeningitis virus, exhibiting hyperactivation of CTLs and antigen-presenting cells, and inadequate restriction of viral proliferation. In contrast, neither Listeria monocytogenes nor MCMV induces the syndrome. In mice, the HLH phenotype is conditional, which suggests the existence of a specific infectious trigger of FHL3 in humans
Erratum: ‘‘Picosecond large‐signal switching characteristics of a pseudomorphic AlGaAs/InGaAs modulation‐doped field‐effect transistor’’ [Appl. Phys. Lett. 61, 1187 (1992)]
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/70138/2/APPLAB-61-26-3194-1.pd
Picosecond large‐signal switching characteristics of a pseudomorphic AlGaAs/InGaAs modulated doped field effect transistor
We present the first comprehensive study of the large‐signal switching characteristics of an AlGaAs/InGaAs modulation‐doped field‐effect transistor on a picosecond time scale. Electro‐optic sampling is used to measure drain voltage response to a steplike gate input with a 2.8 ps rise time, at various dc biases. A large‐signal switching time of 6.2 ps is obtained. Features deleterious to high‐frequency device operation are observed, related to equivalent circuit parameters, and reduced by appropriate choice of operating point.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/69803/2/APPLAB-61-10-1187-1.pd
Hypopigmentation and Maternal-Zygotic Embryonic Lethality Caused by a Hypomorphic Mbtps1 Mutation in Mice
The site 1 protease, encoded by Mbtps1, mediates the initial cleavage of site 2 protease substrates, including sterol regulatory element binding proteins and CREB/ATF transcription factors. We demonstrate that a hypomorphic mutation of Mbtps1 called woodrat (wrt) caused hypocholesterolemia, as well as progressive hypopigmentation of the coat, that appears to be mechanistically unrelated. Hypopigmentation was rescued by transgenic expression of wild-type Mbtps1, and reciprocal grafting studies showed that normal pigmentation depended upon both cell-intrinsic or paracrine factors, as well as factors that act systemically, both of which are lacking in wrt homozygotes. Mbtps1 exhibited a maternal-zygotic effect characterized by fully penetrant embryonic lethality of maternal-zygotic wrt mutant offspring and partial embryonic lethality (~40%) of zygotic wrt mutant offspring. Mbtps1 is one of two maternal-zygotic effect genes identified in mammals to date. It functions nonredundantly in pigmentation and embryogenesis
MHC class I–deficient natural killer cells acquire a licensed phenotype after transfer into an MHC class I–sufficient environment
In MHC class I–deficient hosts, natural killer (NK) cells are hyporesponsive to cross-linking of activation receptors. Functional competence requires engagement of a self–major histocompatability complex (MHC) class I–specific inhibitory receptor, a process referred to as “licensing.” We previously suggested that licensing is developmentally determined in the bone marrow. In this study, we find that unlicensed mature MHC class I–deficient splenic NK cells show gain-of-function and acquire a licensed phenotype after adoptive transfer into wild-type (WT) hosts. Transferred NK cells produce WT levels of interferon-γ after engagement of multiple activation receptors, and degranulate at levels equivalent to WT NK cells upon coincubation with target cells. Only NK cells expressing an inhibitory Ly49 receptor specific for a cognate host MHC class I molecule show this gain-of-function. Therefore, these findings, which may be relevant to clinical bone marrow transplantation, suggest that neither exposure to MHC class I ligands during NK development in the BM nor endogenous MHC class I expression by NK cells themselves is absolutely required for licensing
Found in translation: the human equivalent of mouse CD8+ dendritic cells
The murine dendritic cell network comprises multiple subsets with distinct functions, but few of their human counterparts have been described. New data now reveals the likely human equivalent of the mouse DC subset specialized in cross-presentation
Development of a mouse monoclonal antibody for the detection of asymmetric dimethylarginine of Translocated in LipoSarcoma/FUsed in Sarcoma and its application in analyzing methylated TLS
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