PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL'S WEBSITE.
**********************************************NATURE MATERIALS**************************************(http://www.nature.com/naturematerials)
[1] Room-temperature spintronics
DOI: 10.1038/nmat984 (http://dx.doi.org/10.1038/nmat984)
In today's information world, bits of data are processed by semiconductor chips, and stored in magnetic disk drives. But tomorrow's information technology may see magnetism and semiconductivity combined in one 'spintronic' device that exploits both charge and 'spin' to carry data. In the October issue of Nature Materials, Rao and colleagues describe a material — known as a dilute magnetic semiconductor — that displays the desired semiconducting and magnetic properties, and, crucially, does so when operating above room temperature.
The potential advantages — higher speed, greater efficiency, better stability — of spintronic devices makes finding a material with both semiconducting and ferromagnetic properties very important. Three years ago, theoreticians predicted that the semiconductors ZnO and GaN would become ferromagnetic above room temperature when doped with a small amount of the magnetic impurity, Mn. Since then, experimentalists have been busy trying to synthesize semiconductors having magnetic behaviour over this useful temperature range.
Rao and colleagues report the first observations of ferromagnetism above room temperature in ZnO doped with Mn — in bulk, thin film or powder form. The authors attribute their success to the low temperatures used to fabricate the material; samples synthesized at higher temperatures were not ferromagnetic at room temperature. The possibility of using electric and magnetic fields (as well as light) to process and store information in these materials makes future spintronic devices based on Mn-doped ZnO very attractive.
Other papers from Nature Materials to be published online at the same time and with the same embargo:
[2] Solution-processed ambipolar organic field-effect transistors and inverters(DOI: 10.1038/nmat978) (http://dx.doi.org/10.1038/nmat978)
[3] The distribution of glass-transition temperatures in nanoscopically confined glass formers(DOI: 10.1038/nmat980) (http://dx.doi.org/10.1038/nmat980)
[4] Cobalt-based bulk glassy alloy with ultrahigh strength and soft magnetic properties(DOI: 10.1038/nmat982) (http://dx.doi.org/10.1038/nmat982)
[5] Assembling a lasing hybrid material with supramolecular polymers and nanocrystals(DOI: 10.1038/nmat983) (http://dx.doi.org/10.1038/nmat983)
*******************************************NATURE BIOTECHNOLOGY*********************************(http://www.nature.com/naturebiotechnology)
[6] Therapeutic cloning in parkinsonian mice
DOI: 10.1038/nbt870 (http://dx.doi.org/10.1038/nbt870)
In the first example of therapeutic cloning for treating a brain disorder, Lorenz Studer and colleagues have used dopamine neurons derived from cloned mouse embryonic stem (ES) cells to treat mice with a Parkinson-like condition. The study, published in the October issue of Nature Biotechnology, is only the second report of therapeutic cloning in animals.
A loss of dopamine neurons is a hallmark of Parkinson disease. Dopamine neurons derived from ES cells were previously shown to be effective in treating parkinsonian mice. But the cells in this earlier study expressed a transgene—raising safety concerns—and they had not been generated by cloning.
The goal of therapeutic cloning is to produce specialized cells needed to repair a failing organ from human ES cells generated by cloning the patient's own cells. Unlike generic ES cells, such cloned ES cells and their specialized progeny would be genetically identical to the patient and could be transplanted without being rejected by the patient's immune system. Although therapeutic cloning has great promise for treating many diseases, it has not yet been demonstrated in human patients.
**********************************************NATURE GENETICS****************************************(http://www.nature.com/naturegenetics)
[7] Gene associated with susceptibility to common form of stroke
DOI: 10.1038/ng1245 (http://dx.doi.org/10.1038/ng1245) Scientists at deCODE Genetics in Iceland report in the October issue of Nature Genetics that they have identified a gene that is associated with susceptibility to stroke. Stroke is the third leading cause of death in western countries, and more than 600,000 individuals suffer a stroke each year in the United States.
Solveig Gretarsdottir and colleagues at deCODE had previously mapped a stroke-susceptibility gene to a region on chromosome 5. In the present study, they report a large-scale effort to identify the gene in question involving several hundred people in Iceland who had suffered a stroke. The strongest association was found for the gene PDE4D, linked to susceptibility to ischemic stroke, which is how 80"90% of all strokes are classified. Although there are no variants in the gene itself that are associated with stroke, the authors did show that three different isoforms of the gene were expressed at lower levels in those affected by the disease. Certain combinations of variants in regions flanking the gene were associated with higher or lower risk of stroke.
The gene PDE4D encodes an enzyme called a phosphodiesterase, which breaks down cyclic AMP, a molecule with many biological roles. As defined in animal studies, one such role is in the proliferation and migration of vascular cells, which may be involved in promoting atherosclerosis, a key risk factor for stroke. Gretarsdottir and colleagues suggest that drugs targeting this phosphodiesterase in the at-risk population may prove to be beneficial. Phosphodiesterase inhibitors are already being used to treat asthma, inflammation, and erectile dysfunction (Viagra).
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[8] Spontaneous activity of opsin apoprotein is a cause of Leber congenital amaurosis(DOI: 10.1038/ng1246) (http://dx.doi.org/10.1038/ng1246)
[9] Partial deficiency of the C-terminal-domain phosphatase of RNA polymerase II is associated with congenital cataracts facial dysmorphism neuropathy syndrome(DOI: 10.1038/ng1243) (http://dx.doi.org/10.1038/ng1243)
[10] The beta-globin nuclear compartment in development and erythroid differentiation(DOI: 10.1038/ng1244) (http://dx.doi.org/10.1038/ng1244)
*********************************************NATURE NEUROSCIENCE*********************************(http://www.nature.com/natureneuroscience)
[11] How HIV infection kills brain cells
DOI: 10.1038/nn1127 (http://dx.doi.org/10.1038/nn1127)
People infected with the human immunodeficiency virus type 1 (HIV-1) may develop dementia due to the death of neurons in the brain. However, HIV-1 does not infect neurons, suggesting that an indirect process is at work. A potent neurotoxin produced by a complex interaction of signals from non-neuronal brain cells may be the answer, reports a study in the October issue of Nature Neuroscience. This work suggests that drugs already in clinical trials for another disease may be effective for treating HIV-associated dementia.
The authors found that when certain immune cells (called macrophages) were infected with HIV-1, they released a substance toxic to neurons. Further examination revealed that the substance, an inactive form of a protein called matrix metalloprotease 2 (MMP2), was itself not the killer, but rather was converted by neurons into an enzyme that cleaves another protein, called stromal-derived factor (SDF) 1. SDF-1 has a number of normal functions in the brain, but the shortened form of SDF-1 was highly toxic to neurons. Rats given the inactive MMP2 showed loss of neurons and exhibited behavioral problems. By using drugs that block the activation of MMP2 (and thus the cleavage of SDF-1), the researchers could diminish the toxic effects. Such MMP2 inhibitors are already in clinical trials for cancer.
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[12] Cdk5 activation induces hippocampal CA1 cell death by directly phosphorylating NMDA receptors (DOI: 10.1038/nn1119) (http://dx.doi.org/10.1038/nn1119)
[13] In vitro formation of a secondary epileptogenic mirror focus by interhippocampal propagation of seizures (DOI: 10.1038/nn1125) (http://dx.doi.org/10.1038/nn1125) [14] Brief presynaptic bursts evoke synapse-specific retrograde inhibition mediated by endogenous cannabinoids (DOI: 10.1038/nn1126) (http://dx.doi.org/10.1038/nn1126) [15] Regulation of acetylcholine receptor clustering by the tumor suppressor APC (DOI: 10.1038/nn1128) (http://dx.doi.org/10.1038/nn1128)
*********************************************NATURE IMMUNOLOGY************************************(http://www.nature.com/natureimmunology)
[16] Persistent infection impairs the immune system
DOI: 10.1038/ni975 (http://dx.doi.org/10.1038/ni975)
Defective T cell responses are a common feature of patients with certain infectious diseases, autoimmune disorders and cancers that differ widely in their causes and symptoms. In the October issue of Nature Immunology scientists have now identified persistent infection as the major factor linking these diverse pathologies.
Michal Baniyash and colleagues from Hebrew University, Israel, hypothesized that persistent exposure to antigen could account for the impaired T cell responses observed in different diseases. Animals persistently exposed to bacteria had poor T cell responses—examination of the T cell receptor complex showed defective zeta chain expression on the cell surface. Importantly, chronic bacterial infection reduced the ability of the animal to fight influenza infection. The authors hypothesize that zeta chain down-regulation could be a physiological mechanism that helps prevent overblown immune responses. However, it can act as a double-edged sword by impairing the ability to respond adequately to chronic diseases.
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[17] Cross-priming of CD8+ T cells stimulated by virus-induced type I interferon (DOI: 10.1038/ni978) (http://dx.doi.org/10.1038/ni978)
[18] The inter-relatedness and interdependence of mouse T cell receptor gammadelta+ and alphabeta+ cells (DOI: 10.1038/ni979) (http://dx.doi.org/10.1038/ni979)
***************************************************************************************************************Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE (http://www.nature.com)
[19] Basal body dysfunction probably underlies the pleiotropic phenotype of Bardet-Biedl syndrome (DOI: 10.1038/nature02030) (http://dx.doi.org/10.1038/nature02030)
NATURE MEDICINE (http://www.nature.com/naturemedicine)
[20] Natural antibodies and complement are endogenous adjuvants for vaccine-induced CD8+ T-cell responses(DOI: 10.1038/nm933) (http://dx.doi.org/10.1038/nm933)
[21] Inhibition of renal cystic disease development and progression by a vasopressin V2 receptor antagonist (DOI: 10.1038/nm935) (http://dx.doi.org/10.1038/nm935)
[22] Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine-2,3-dioxygenase (DOI: 10.1038/nm934) (http://dx.doi.org/10.1038/nm934)
[23] Monitoring photodynamic therapy of solid tumors online by BOLD-contrast MRI (DOI: 10.1038/nm940) (http://dx.doi.org/10.1038/nm940)
NATURE STRUCTURAL BIOLOGY (http://www.nature.com/naturestructuralbiology)
[24] Structure and autoregulation of the yeast Hst2 homolog of Sir2 (DOI: 10.1038/nsb978) (http://dx.doi.org/10.1038/nsb978)
[25] A structural model for actin-induced nucleotide release in myosin (DOI: 10.1038/nsb987) (http://dx.doi.org/10.1038/nsb987)
[26] Myosin cleft movement and its coupling to actomyosin dissociation (DOI: 10.1038/nsb986) (http://dx.doi.org/10.1038/nsb986)
[27] Context and conformation dictate function of a transcription antitermination switch (DOI: 10.1038/nsb983) (http://dx.doi.org/10.1038/nsb983)
***************************************************************************************************************
GEOGRAPHICAL LISTING OF AUTHORS
The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.
AUSTRALIAPerth: 9
AUSTRIAVienna: 9
BELGIUMBrussels: 22
BULGARIASofia: 9
CANADABurnaby: 19Calgary: 11, 12Vancouver: 11
CHINAChangchun: 27Tianjin: 5
FRANCEGrenoble: 4Lyon: 17Marseilles: 13
GERMANYBerlin: 9Hannover: 25Heidelberg: 25Munich: 9Wuppertal: 2
HUNGARYBudapest: 26
ICELANDReykjavik: 7
ISRAELJerusalem: 16Rehovot: 23
ITALYBologna: 9
JAPANSendai: 1, 4
THE NETHERLANDSAmsterdam: 9, 20Delft: 2Eindhoven: 2Groningen: 2Rotterdam: 10
SAUDI ARABIARiyadh: 19
SOUTH AFRICACape Town: 20
SWEDENStockholm: 1Uppsala: 1
SWITZERLANDBasel: 7
UNITED KINGDOMCambridge: 17Glasgow: 20Leicester: 26London: 9, 18, 19, 20Newbury: 17Sheffield: 1Stevenage: 18
UNITED STATES OF AMERICA
Arizona Tampe: 1California Los Angeles: 8 Oakland: 9 Pasadena: 27 Stanford: 9, 14Connecticut New Haven: 18 Storrs: 6Florida Tallahassee: 26Georgia Atlanta: 18Illinois Evanston: 3, 5Indiana Indianapolis: 21Kansas Lawrence: 25Maryland Baltimore: 17 Bethesda: 8, 26Massachusetts Boston: 8, 14Minnesota Rochester: 21New Hampshire Hanover: 25 Lebanon: 13New Jersey Picatinny: 1New York New York: 6Pennsylvania Philadelphia: 24 Pittsburgh: 15Texas Houston: 19Utah Salt Lake City: 9Washington Seattle: 9
PRESS CONTACTS"¦
Nature Publishing Group is a division of Macmillan Publishers Ltd.
Macmillan is an international publisher serving the information and education community as well as publishing fiction and non-fiction.
RSS