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  • 1
    Publication Date: 2011-05-27
    Description: The electron is predicted to be slightly aspheric, with a distortion characterized by the electric dipole moment (EDM), d(e). No experiment has ever detected this deviation. The standard model of particle physics predicts that d(e) is far too small to detect, being some eleven orders of magnitude smaller than the current experimental sensitivity. However, many extensions to the standard model naturally predict much larger values of d(e) that should be detectable. This makes the search for the electron EDM a powerful way to search for new physics and constrain the possible extensions. In particular, the popular idea that new supersymmetric particles may exist at masses of a few hundred GeV/c(2) (where c is the speed of light) is difficult to reconcile with the absence of an electron EDM at the present limit of sensitivity. The size of the EDM is also intimately related to the question of why the Universe has so little antimatter. If the reason is that some undiscovered particle interaction breaks the symmetry between matter and antimatter, this should result in a measurable EDM in most models of particle physics. Here we use cold polar molecules to measure the electron EDM at the highest level of precision reported so far, providing a constraint on any possible new interactions. We obtain d(e) = (-2.4 +/- 5.7(stat) +/- 1.5(syst)) x 10(-28)e cm, where e is the charge on the electron, which sets a new upper limit of |d(e)| 〈 10.5 x 10(-28)e cm with 90 per cent confidence. This result, consistent with zero, indicates that the electron is spherical at this improved level of precision. Our measurement of atto-electronvolt energy shifts in a molecule probes new physics at the tera-electronvolt energy scale.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hudson, J J -- Kara, D M -- Smallman, I J -- Sauer, B E -- Tarbutt, M R -- Hinds, E A -- England -- Nature. 2011 May 26;473(7348):493-6. doi: 10.1038/nature10104.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cold Matter, Blackett Laboratory, Imperial College London, Prince Consort Road, London SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21614077" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2012-09-08
    Description: Autism spectrum disorders are a genetically heterogeneous constellation of syndromes characterized by impairments in reciprocal social interaction. Available somatic treatments have limited efficacy. We have identified inactivating mutations in the gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with autism, epilepsy, and intellectual disability. The encoded protein is responsible for phosphorylation-mediated inactivation of the E1alpha subunit of branched-chain ketoacid dehydrogenase (BCKDH). Patients with homozygous BCKDK mutations display reductions in BCKDK messenger RNA and protein, E1alpha phosphorylation, and plasma branched-chain amino acids. Bckdk knockout mice show abnormal brain amino acid profiles and neurobehavioral deficits that respond to dietary supplementation. Thus, autism presenting with intellectual disability and epilepsy caused by BCKDK mutations represents a potentially treatable syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704165/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novarino, Gaia -- El-Fishawy, Paul -- Kayserili, Hulya -- Meguid, Nagwa A -- Scott, Eric M -- Schroth, Jana -- Silhavy, Jennifer L -- Kara, Majdi -- Khalil, Rehab O -- Ben-Omran, Tawfeg -- Ercan-Sencicek, A Gulhan -- Hashish, Adel F -- Sanders, Stephan J -- Gupta, Abha R -- Hashem, Hebatalla S -- Matern, Dietrich -- Gabriel, Stacey -- Sweetman, Larry -- Rahimi, Yasmeen -- Harris, Robert A -- State, Matthew W -- Gleeson, Joseph G -- K08 MH087639/MH/NIMH NIH HHS/ -- K08MH087639/MH/NIMH NIH HHS/ -- P01 HD070494/HD/NICHD NIH HHS/ -- P01HD070494/HD/NICHD NIH HHS/ -- P30 NS047101/NS/NINDS NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 NS041537/NS/NINDS NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01NS048453/NS/NINDS NIH HHS/ -- R25 MH077823/MH/NIMH NIH HHS/ -- RC2 MH089956/MH/NIMH NIH HHS/ -- RC2MH089956/MH/NIMH NIH HHS/ -- T32MH018268/MH/NIMH NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):394-7. doi: 10.1126/science.1224631. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA. gnovarino@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956686" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)/*administration & ; dosage/deficiency/*genetics ; Adolescent ; Amino Acids, Branched-Chain/administration & dosage/blood/deficiency ; Animals ; Arginine/genetics ; Autistic Disorder/*diet therapy/enzymology/*genetics ; Base Sequence ; Brain/metabolism ; Child ; Child, Preschool ; Diet ; Epilepsy/*diet therapy/enzymology/*genetics ; Female ; Homozygote ; Humans ; Intellectual Disability/diet therapy/enzymology/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Pedigree ; Phosphorylation ; Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/metabolism ; Young Adult
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-02-01
    Description: Hereditary spastic paraplegias (HSPs) are neurodegenerative motor neuron diseases characterized by progressive age-dependent loss of corticospinal motor tract function. Although the genetic basis is partly understood, only a fraction of cases can receive a genetic diagnosis, and a global view of HSP is lacking. By using whole-exome sequencing in combination with network analysis, we identified 18 previously unknown putative HSP genes and validated nearly all of these genes functionally or genetically. The pathways highlighted by these mutations link HSP to cellular transport, nucleotide metabolism, and synapse and axon development. Network analysis revealed a host of further candidate genes, of which three were mutated in our cohort. Our analysis links HSP to other neurodegenerative disorders and can facilitate gene discovery and mechanistic understanding of disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157572/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157572/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novarino, Gaia -- Fenstermaker, Ali G -- Zaki, Maha S -- Hofree, Matan -- Silhavy, Jennifer L -- Heiberg, Andrew D -- Abdellateef, Mostafa -- Rosti, Basak -- Scott, Eric -- Mansour, Lobna -- Masri, Amira -- Kayserili, Hulya -- Al-Aama, Jumana Y -- Abdel-Salam, Ghada M H -- Karminejad, Ariana -- Kara, Majdi -- Kara, Bulent -- Bozorgmehri, Bita -- Ben-Omran, Tawfeg -- Mojahedi, Faezeh -- Mahmoud, Iman Gamal El Din -- Bouslam, Naima -- Bouhouche, Ahmed -- Benomar, Ali -- Hanein, Sylvain -- Raymond, Laure -- Forlani, Sylvie -- Mascaro, Massimo -- Selim, Laila -- Shehata, Nabil -- Al-Allawi, Nasir -- Bindu, P S -- Azam, Matloob -- Gunel, Murat -- Caglayan, Ahmet -- Bilguvar, Kaya -- Tolun, Aslihan -- Issa, Mahmoud Y -- Schroth, Jana -- Spencer, Emily G -- Rosti, Rasim O -- Akizu, Naiara -- Vaux, Keith K -- Johansen, Anide -- Koh, Alice A -- Megahed, Hisham -- Durr, Alexandra -- Brice, Alexis -- Stevanin, Giovanni -- Gabriel, Stacy B -- Ideker, Trey -- Gleeson, Joseph G -- HHSN268200782096C/PHS HHS/ -- HHSN268201100011/PHS HHS/ -- N01-CO-12400/CO/NCI NIH HHS/ -- P01 HD070494/HD/NICHD NIH HHS/ -- P01HD070494/HD/NICHD NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01NS041537/NS/NINDS NIH HHS/ -- R01NS048453/NS/NINDS NIH HHS/ -- R01NS052455/NS/NINDS NIH HHS/ -- U54 HG006504/HG/NHGRI NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- U54HG006504/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):506-11. doi: 10.1126/science.1247363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Biological Transport/genetics ; Cohort Studies ; Exome/*genetics ; Gene Regulatory Networks ; *Genetic Association Studies ; Humans ; Motor Neuron Disease/*genetics ; Mutation ; Neurons/*metabolism ; Nucleotides/genetics/metabolism ; Pyramidal Tracts/*metabolism ; Sequence Analysis, DNA ; Spastic Paraplegia, Hereditary/*genetics ; Synapses/physiology ; Transcriptome ; Zebrafish
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The role of G protein mutations in the pathogenesis of adrenal cortex neoplasms is controversial. Two published studies disagree on the existence of a cysteine or histidine for arginine substitution at position 179 (R179C/H) of the GTP binding region of the α chain of an inhibitory G protein (Gi2α) in these tumors. Prior studies using detection by mutation-specific oligonucleotide hybridization showed either 3 of 11 or 0 of 56 tumors harbored mutations. To resolve this discrepancy and ascertain the importance of the R179C/H Gi2α mutation in the development of adrenal cortex tumors, we screened tumors from 29 patients (24 with adenoma, 5 with carcinoma) using a more sensitive assay employing polymerase chain reaction (PCR) and examination for restriction fragment length polymorphisms (RFLP). Detection of the potential R179C/H mutation by this technique was possible because the wild-type coding sequence includes the BSTU-1 restriction endonuclease recognition site CGCG, whereas the mutated gene does not. Results showed complete digestion of the amplified DNA samples from all 29 patients and the negative control DNA by BSTU-1, indicating that all tumor samples exhibited only the wild-type sequence. Direct sequencing of PCR product from four tumor samples confirmed the presence of only the wild-type sequence. The 0 of 29 rate of R179C/H mutations we found in Gi2α is different than the 3 of 11 positive rate ( p 〈 0.05, Fishers’ exact) previously reported but agrees with the report showing 0 of 56 mutations. We conclude a mutation at position 179 of Gi 2 α is not important in the pathogenesis of most adrenal cortical tumors.
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  • 5
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé On a observé des altérations des plaques d'adhésion dans certaines lignées cellulaires transformées, et celles-ci semblent être associées à un potentiel métastatique augmenté. La plaque d'adhésion prototypique est formée par des récepteurs α5β1 de fibronectine (FnR) qui agissent sur le réseau cellulaire d'actine. Nous avons trouvé une différence entre les réseaux d'actine des clones noninvasifs (FTC-133) et invasifs (FTC-236, FTC-238) des lignées cellulaires dans le cancer folliculaire de la thyroïde chez l'homme. La TSH induit des fibres de stress dans le FTC-133. Afin d'évaluer les différences dans les plaques d'adhésion, l'expression de la fibronectine (FN) et de son récepteur ont été analysées. Pour ces études, les clones FTC-133, FTC-236 et FTC-238 ont été mis en culture dans le milieu DME-H21 dépourvu en sérum pendant 24 heures avant l'addition de 30 mU/ml de TSH/24 heures. II n'y avait aucune différence quantitative dans l'expression FN sur “Western blot” que ce soit sur le milieu ainsi conditionné ou sur les extraits cellulaires. Les “Western blots” et les études immunohistochimiques ont indiqué que la TSH n'induisait la sécrétion de FN que dans la lignée FTC-133. La cytométrie de flux avec l'anticorps α5 a démontré une réduction respectivement de 52% et de 45% (p〈0.01) dans l'expression de FnR par les clones FTC-236 et FTC-238, comparé au FTC-133. Cette donnée a été confirmée par l'immunohistochimie. A partir de ces études, nous concluons que les clones d'invasion de FTC diminuent leur expression en FnR sans changer leur expression de FN. De plus, un traitement par la TSH peut induire la sécrétion de FN par le clone FTC-133 alors qu'il ne semble pas influencer le FnR ou l'expression FN. L'expression diminuée des plaques d'adhésion FnR semble potentialiser les métastases dans certains cancers de la thyroïde.
    Abstract: Resumen Se han observado placas adhesivas alteradas en líneas celulares transformadas en asociación con un potencial metastásico incrementado. La prototípica placa adhesiva se forma por la interacción de receptores α5-β1 con la trama celular de actina. Hemos encontrado diferencias en las tramas de actina en clones no invasivos (FTC-133) e invasivos (FTC-236, FTC-238) de una línea celular de cáncer folicular de tiroides. Además, la TSH induce líneas de estrés en FTC-133. Con el objeto de investigar las diferencias en las placas adhesivas, se hizo el análisis de la expresión de fibronectina (FN) y sus receptores en tales células. Para estos estudios se hizo el cultivo de FTC-133, FTC-236 y FTC-238, en sueros depletados de DME-H21 por 24 horas anteriores a la adición de 30 mU/ml TSH por 24 horas. No se observaron diferencias cuantitativas en la expresion de FN o en el Western blot ni en los medios condicionados ni en los extractos celulares. Los Western blots y los estudios inmunohistoquímicos indicaron que la TSH induce la secreción de FN sólo en FTC-133. La citometría de flujo con un anticuerpo α5 demostró una reducción de 52% y 45% (p〈0.01) en la expresión de FnR por FTC-236 y FT-238, respectivamente, en comparación con FTC-133; este hallazgo fue verificado por inmuno-histoquímica. El tratamiento con TSH no alteró la expresón FnR. Con base en estos estudios, es nuestra conclusión que los clones invasivos de FTC disminuyen la expresión de FnR sin cambiar su expresión de FN. Además, el tratamiento con TSH puede promover la secreciòn de FN por FTC-133, aunque no parece afectar la expresión de FnR o la expresión absoluta de FN. Esta expresión disminuída de las placas adhesivas FnR puede incrementar el potencial metastásico en algunos cánceres foliculares de tiroides.
    Notes: Abstract Altered adhesion plaques have been observed in transformed cell lines and are associated with enhanced metastatic potential. The prototypical adhesion plaque is formed by α5β1 fibronectin receptors (FnRs) interacting with the cellular actin network. We have found differences in the actin networks of noninvasive (FTC-133) and invasive (FTC-236, FTC-238) clones of a human follicular thyroid cancer cell line. Furthermore, thyroid-stimulating hormone (TSH) induces stress fibers in FTC-133. In order to investigate differences in adhesion plaques, expression of fibronectin (FN) and its receptor by these cells was analyzed. For these studies FTC-133, FTC-236, and FTC-238 were cultured in serum-depleted DME-H21 medium for 24 hours before the addition of TSH 30 mU/ml. No quantitative differences were noted in FN expression on Western blot in either the conditioned medium or cellular extracts. Western blots and immunohistochemical studies indicated that TSH induced secretion of FN only in FTC-133. Flow cytometry with an α5 antibody demonstrated a 52% and 45% reduction (p〈0.01) in expression of FnR by FTC-236 and FTC-238, respectively, compared to FTC-133; this finding was supported by immunohistochemistry results. TSH treatment did not alter FnR expression. From these studies, we conclude that invasive clones of FTC decrease their expression of FnRs without changing their expression of FN. Furthermore, TSH treatment may promote FN secretion by FTC-133, although it does not seem to affect FnR or absolute FN expression. The diminished expression of FnR adhesion plaques may enhance metastatic potential in some follicular thyroid cancers.
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  • 6
    ISSN: 1430-4171
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract We describe in this paper a set of computer-based simulations for use in general chemistry courses. We detail a discovery-based method of teaching, whereby students are led to discover concepts through guided-inquiry use of the simulation modules. Three methods of using the software are described, as is the development process we have employed. Finally, we describe our evaluation studies of the effects of our methodology and the use of a scientific reasoning instrument. The software is available free for download as part of this article.
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  • 7
    ISSN: 1430-4171
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract This paper reviews a project conducted as part of a general chemistry course. The primary goal of the assignment was to involve our students in the process of teaching chemistry. Our work is part of STEMTEC, the Science, Technology, Engineering, and Mathematics Teacher Education Collaborative, which has been developed to improve the preparation of preservice teachers, stimulate the interest of undergraduate science and mathematics majors in the teaching profession, and increase the educational effectiveness of science and mathematics courses. The assigned project required students to create an interactive computer module that could be used to educate other students about concepts taught in general chemistry. The paper includes examples of these modules and evaluates this method of instruction. The software programs designed by the students are available for download from the Internet (http://soulcatcher.chem.umass.edu).
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  • 8
    ISSN: 1432-0584
    Keywords: Key words Pyomyositis ; Non-Hodgkin's lymphoma ; Chemotherapy ; Splenectomy ; Abscess
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Pyomyositis is a rare disease, encountered mainly in tropical climates. The diagnosis of this entity is difficult, if not misdiagnosed, because of its rarity and its subacute presentation. We report of a 42-year-old man, in whom pyomyositis developed while he was receiving the standard chemotherapy for T-cell non-Hodgkin's lymphoma (NHL). Three months following splenectomy, multiple abscesses occurred in the muscles of both thighs while the patient was receiving the third course of the CHOP regimen. A purulent exudate was aspirated from the abscesses under computed tomographic guidance. Coagulase-positive Staphylococcus aureus was cultured in the aspirate. Pyomyositis was completely resolved following the surgical drainage and the antistaphylococcal antibiotic treatment. This patient has shown that immunosuppression due to splenectomy, NHL, and chemotherapy, especially when using steroids, could be risk factors for pyomyositis in nontropical or semitropical countries.
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  • 9
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the cytotoxic T lymphocyte antigen 4 gene (CTLA4)—which encodes a vital negative regulatory molecule of ...
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  • 10
    Electronic Resource
    Electronic Resource
    [S.l.] : International Union of Crystallography (IUCr)
    Acta crystallographica 37 (1981), S. 201-210 
    ISSN: 1600-5724
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Notes: A rigorous treatment of the constraints imposed by site and body symmetry on the orientational distribution of librating molecules is presented in terms of multipole expansions. Radial densities of the site-symmetric dynamic multipole expansion are linear combinations of the radial densities of the body-symmetric static multipole expansion of the same multipole order. The transformation from static to dynamic radial densities is transmitted by libration matrices, which can be included as parameters in a structure factor model. The matrix elements are connected to the rotational dynamics of the molecule. They are expansion coefficients of the orientational distribution in a basis obtained by site and body symmetrization of the real Wigner functions. Both symmetrizations are reduced to selecting terms from a general basis according to simple index rules. Independence of the kind of density function and Fourier invariance make the formalism useful in combined neutron and X-ray diffraction studies.
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