| 1. |
- Claesson, Thomas, et al.
(author)
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Angle Resolved Photoemission from Nd(1.85)Ce(0.15)CuO(4) using High Energy Photons : A Fermi Surface Investigation
- 2004
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In: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 93:13, s. 136402-1-136402-4
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Journal article (peer-reviewed)abstract
- We have performed an angle resolved photoemission study on a single crystal of the optimally electron doped (n-type) cuprate superconductor Nd2-xCexCuO4 (x=0.15) at a photon energy of 400 eV. The Fermi surface is mapped out and is, in agreement with earlier measurements, of hole-type with the expected Luttinger volume. However, comparing with previous low energy measurements, we observe a different Fermi surface shape and a different distribution of spectral intensity around the Fermi surface contour. The observed Fermi surface shape indicates a stronger electron correlation in the bulk as compared to the surface.
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| 2. |
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| 3. |
- Kullander, Klas, et al.
(author)
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Ephrin-B3 is the midline barrier that prevents corticospinal tract axons from recrossing, allowing for unilateral motor control
- 2001
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In: Genes & Development. - : Cold Spring Harbor Laboratory. - 0890-9369 .- 1549-5477. ; 15:7, s. 877-888
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Journal article (peer-reviewed)abstract
- Growing axons follow highly stereotypical pathways, guided by a variety of attractive and repulsive cues, before establishing specific connections with distant targets. A particularly well-known example that illustrates the complexity of axonal migration pathways involves the axonal projections of motor neurons located in the motor cortex. These projections take a complex route during which they first cross the midline, then form the corticospinal tract, and ultimately connect with motor neurons in the contralateral side of the spinal cord. These obligatory contralateral connections account for why one side of the brain controls movement on the opposing side of the body. The netrins and slits provide well-known midline signals that regulate axonal crossings at the midline. Herein we report that a member of the ephrin family, ephrin-B3, also plays a key role at the midline to regulate axonal crossing. In particular, we show that ephrin-B3 acts as the midline barrier that prevents corticospinal tract projections from recrossing when they enter the spinal gray matter. We report that in ephrin-B3(-/-) mice, corticospinal tract projections freely recross in the spinal gray matter, such that the motor cortex on one side of the brain now provides bilateral input to the spinal cord. This neuroanatomical abnormality in ephrin-B3(-/-) mice correlates with loss of unilateral motor control, yielding mice that simultaneously move their right and left limbs and thus have a peculiar hopping gait quite unlike the alternate step gait displayed by normal mice. The corticospinal and walking defects in ephrin-B3(-/-) mice resemble those recently reported for mice lacking the EphA4 receptor, which binds ephrin-B3 as well as other ephrins, suggesting that the binding of EphA4-bearing axonal processes to ephrin-B3 at the midline provides the repulsive signal that prevents corticospinal tract projections from recrossing the midline in the developing spinal cord.
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| 4. |
- Margolis, Russell L, et al.
(author)
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Huntington's Disease-like 2 (HDL2) in North America and Japan.
- 2004
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In: Annals of Neurology. - : Wiley. - 0364-5134 .- 1531-8249. ; 56:5, s. 670-4
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Journal article (peer-reviewed)abstract
- Huntington's Disease-like 2 (HDL2) is a progressive, autosomal dominant, neurodegenerative disorder with marked clinical and pathological similarities to Huntington's disease (HD). The causal mutation is a CTG/CAG expansion mutation on chromosome 16q24.3, in a variably spliced exon of junctophilin-3. The frequency of HDL2 was determined in nine independent series of patients referred for HD testing or selected for the presence of an HD-like phenotype in North America or Japan. The repeat length, ancestry, and age of onset of all North American HDL2 cases were determined. The results show that HDL2 is very rare, with a frequency of 0 to 15% among patients in the nine case series with an HD-like presentation who do not have the HD mutation. HDL2 is predominantly, and perhaps exclusively, found in individuals of African ancestry. Repeat expansions ranged from 44 to 57 triplets, with length instability in maternal transmission detected in a repeat of r2=0.29, p=0.0098). The results further support the evidence that the repeat expansion at the chromosome 16q24.3 locus is the direct cause of HDL2 and provide preliminary guidelines for the genetic testing of patients with an HD-like phenotype.
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| 5. |
- Ranius, Thomas, et al.
(author)
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Modeling dead wood in Fennoscandian old-growth forests dominated by Norway spruce
- 2004
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In: Canadian Journal of Forest Research. - 0045-5067 .- 1208-6037. ; 34:5, s. 1025-1034
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Journal article (peer-reviewed)abstract
- If equilibrium is assumed in unmanaged forests, the volume of coarse woody debris (CWD), VCWD, may be calculated from (i) the volume of living trees, Vliving, (ii) average volume of a dead stem in relation to when it was alive, k, (iii) tree mortality rate, m, and (iv) residence time of CWD, t, by the equation VCWD = Vlivingkmt. We parameterized this equation with data from Norway spruce (Picea abies (L.) Karst.) dominated forests in Fennoscandia. The Vliving was assumed to be directly proportional to forest productivity. Tree mortality data were from the National Forest Inventory, while it was difficult to find quantitative data on k and t. The predicted amounts (74–138 m3/ha, with larger amounts in the south) and size distribution (a negative exponential distribution of the number of stems) of CWD corresponded fairly well to averages from field inventories. By using a computer simulation program, the variability in tree mortality, density of living trees, and residence time of CWD were considered. In the simulations, the amount of CWD varied widely between 1-ha plots, especially for individual decay classes. Therefore, this model could be used to predict averages from larger landscapes unaffected by large disturbances, while no model can predict the amount of CWD at individual plots. [ABSTRACT FROM AUTHOR]
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