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Institution

Lund University

EducationLund, Sweden
About: Lund University is a education organization based out in Lund, Sweden. It is known for research contribution in the topics: Population & Cancer. The organization has 42345 authors who have published 124676 publications receiving 5016438 citations. The organization is also known as: Lunds Universitet & University of Lund.


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Journal ArticleDOI
01 Dec 1986-Heredity
TL;DR: In both cases, it is found that in order for gene flow to be significantly reduced over much of the genome, hybrids must be substantially less fit, and the number of genes involved in building the barrier must be so large that the majority of other genes become closely linked to some locus which is under selection.
Abstract: Suppose that selection acts at one or more loci to maintain genetic differences between hybridising populations. Then, the flow of alleles at a neutral marker locus which is linked to these selected loci will be impeded. We define and calculate measures of the barrier to gene flow between two distinct demes, and across a continuous habitat. In both cases, we find that in order for gene flow to be significantly reduced over much of the genome, hybrids must be substantially less fit, and the number of genes involved in building the barrier must be so large that the majority of other genes become closely linked to some locus which is under selection. This conclusion is not greatly affected by the pattern of epistasis, or the position of the marker locus along the chromosome.

641 citations

Journal ArticleDOI
20 Nov 2008-Nature
TL;DR: It is shown that the crystal structure of indium phosphide (InP) nanowires can be controlled by using impurity dopants, and it is demonstrated that zinc decreases the activation barrier for two-dimensional nucleation growth of zinc-blende InP and therefore promotes crystallization of the InPnanowires in the zinc- Blende, instead of the commonly found wurtzite, crystal structure.
Abstract: In most superconductors, the pairing-up of electrons responsible for resistance-free conductivity is driven by vibrations of the solid's crystal lattice. But there are other superconducting materials in which the 'glue' responsible for binding electrons is thought to have a very different origin: quantum fluctuations of spin or charge. An unusually 'violent' generalization of such a pairing mechanisms, in which spin and charge instabilities combine forces, has been identified in the unconventional superconductor CeRhIn5. These intimately coupled fluctuations significantly disrupt the flow of electrons in their normal unpaired state, yet also provide the quantum-mechanical glue necessary for generating superconducting pairs. In this paper, the crystal structure and stacking fault density of semiconducting nanowires composed of the same material are controlled by doping, leading to twinning superlattices. Periodic arrays of rotational dislocations lead to crystal heterostructures in indium phosphide and gallium phosphide nanowires. Semiconducting nanowires offer the possibility of nearly unlimited complex bottom-up design1,2, which allows for new device concepts3,4. However, essential parameters that determine the electronic quality of the wires, and which have not been controlled yet for the III–V compound semiconductors, are the wire crystal structure and the stacking fault density5. In addition, a significant feature would be to have a constant spacing between rotational twins in the wires such that a twinning superlattice is formed, as this is predicted to induce a direct bandgap in normally indirect bandgap semiconductors6,7, such as silicon and gallium phosphide. Optically active versions of these technologically relevant semiconductors could have a significant impact on the electronics8 and optics9 industry. Here we show first that we can control the crystal structure of indium phosphide (InP) nanowires by using impurity dopants. We have found that zinc decreases the activation barrier for two-dimensional nucleation growth of zinc-blende InP and therefore promotes crystallization of the InP nanowires in the zinc-blende, instead of the commonly found wurtzite, crystal structure10. More importantly, we then demonstrate that we can, once we have enforced the zinc-blende crystal structure, induce twinning superlattices with long-range order in InP nanowires. We can tune the spacing of the superlattices by changing the wire diameter and the zinc concentration, and we present a model based on the distortion of the catalyst droplet in response to the evolution of the cross-sectional shape of the nanowires to quantitatively explain the formation of the periodic twinning.

640 citations

Journal ArticleDOI
TL;DR: This review highlights immunological events that may accelerate the development of one of the two diseases in the presence of the co-infecting organism and describes gaps in knowledge and needs for future studies to develop preventive measures against theTwo diseases.
Abstract: Tuberculosis (TB) and HIV co-infections place an immense burden on health care systems and pose particular diagnostic and therapeutic challenges. Infection with HIV is the most powerful known risk factor predisposing for Mycobacterium tuberculosis infection and progression to active disease, which increases the risk of latent TB reactivation 20-fold. TB is also the most common cause of AIDS-related death. Thus, M. tuberculosis and HIV act in synergy, accelerating the decline of immunological functions and leading to subsequent death if untreated. The mechanisms behind the breakdown of the immune defense of the co-infected individual are not well known. The aim of this review is to highlight immunological events that may accelerate the development of one of the two diseases in the presence of the co-infecting organism. We also review possible animal models for studies of the interaction of the two pathogens, and describe gaps in knowledge and needs for future studies to develop preventive measures against the two diseases.

640 citations

Journal ArticleDOI
TL;DR: Bensbyet et al. as discussed by the authors presented abundance trends in the Galactic thin and thick disks for 14 elements (O, Na, Mg, Al, Si, Ca, Ti, Cr, Fe, Ni, Zn, Y, Ba, and Eu).
Abstract: From a detailed elemental abundance analysis of 102 F and G dwarf starswe present abundance trends in the Galactic thin and thick disks for 14elements (O, Na, Mg, Al, Si, Ca, Ti, Cr, Fe, Ni, Zn, Y, Ba, and Eu).Stellar parameters and elemental abundances (except for Y, Ba and Eu)for 66 of the 102 stars were presented in our previous studies (Bensbyet al. 2003, 2004a). The 36 stars that are new in this study extend andconfirm our previous results and allow us to draw further conclusionsregarding abundance trends. The s-process elements Y and Ba, and ther-element Eu have also been considered here for the whole sample for thefirst time. With this new larger sample we now have the followingresults: 1) Smooth and distinct trends that for the thin and thick disksare clearly separated; 2) The alpha-element trends for the thick diskshow typical signatures from the enrichment of SNIa; 3) The thick diskstellar sample is in the mean older than the thin disk stellar sample;4) The thick disk abundance trends are invariant with galactocentricradii (R_m); 5) The thick disk abundance trends appear to be invariantwith vertical distance (Z_max) from the Galactic plane. Adding furtherevidence from the literaure we argue that a merger/interacting scenariowith a companion galaxy to produce a kinematical heating of the stars(that make up today's thick disk) in a pre-existing old thin disk is themost likely formation scenario for the Galactic thick disk.

639 citations

Journal ArticleDOI
TL;DR: The findings suggest that HRPT2 is a tumor-suppressor gene, the inactivation of which is directly involved in predisposition to HPT–JT and in development of some sporadic parathyroid tumors.
Abstract: We report here the identification of a gene associated with the hyperparathyroidism-jaw tumor (HPT-JT) syndrome. A single locus associated with HPT-JT (HRPT2) was previously mapped to chromosomal region 1q25-q32. We refined this region to a critical interval of 12 cM by genotyping in 26 affected kindreds. Using a positional candidate approach, we identified thirteen different heterozygous, germline, inactivating mutations in a single gene in fourteen families with HPT-JT. The proposed role of HRPT2 as a tumor suppressor was supported by mutation screening in 48 parathyroid adenomas with cystic features, which identified three somatic inactivating mutations, all located in exon 1. None of these mutations were detected in normal controls, and all were predicted to cause deficient or impaired protein function. HRPT2 is a ubiquitously expressed, evolutionarily conserved gene encoding a predicted protein of 531 amino acids, for which we propose the name parafibromin. Our findings suggest that HRPT2 is a tumor-suppressor gene, the inactivation of which is directly involved in predisposition to HPT-JT and in development of some sporadic parathyroid tumors.

638 citations


Authors

Showing all 42777 results

NameH-indexPapersCitations
Yi Chen2174342293080
Fred H. Gage216967185732
Kari Stefansson206794174819
Mark I. McCarthy2001028187898
Ruedi Aebersold182879141881
Jie Zhang1784857221720
Feng Zhang1721278181865
Martin G. Larson171620117708
Michael Snyder169840130225
Unnur Thorsteinsdottir167444121009
Anders Björklund16576984268
Carl W. Cotman165809105323
Dennis R. Burton16468390959
Jaakko Kaprio1631532126320
Panos Deloukas162410154018
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023246
2022698
20216,295
20206,032
20195,584
20185,249