32 research outputs found

    USDA Beef Carcass Grades: Purpose and Application.

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    Discrimination between Nuclear Recoils and Electron Recoils by Simultaneous Detection of Phonons and Scintillation Light

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    We have developed a detector, consisting of a cryogenic calorimeter with a scintillating crystal as absorber, and a second calorimeter for the detection of the scintillation light, both operated at 12 mK. Using a CaWO4 crystal with a mass of 6g as scintillating absorber, we have achieved a discrimination of nuclear recoils against electron recoils with a suppression factor of 99.7% at energies above 15 keV. This novel method will be applied for background rejection in the CRESST (Cryogenic Rare Event Search with Superconducting Thermometers) experiment looking for dark matter Weakly Interacting Massive Particles (WIMPs).Comment: 10 pages, 4 zipped figures (not good res.

    The CRESST Dark Matter Search

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    The current status of CRESST (Cryogenic Rare Event Search using Superconducting Thermometers) and new results concerning the detector development are presented. The basic technique of CRESST is to search for particle Dark Matter (WIMPS, Weakly Interacting Massive particles) by the measurement of non-thermal phonons as created by WIMP-induced nuclear recoils. Combined with the newly developed method of simultaneous measurement of scintillation light, strong background discrimination is possible, resulting in a substantial increase in WIMP detection sensitivity. The short and long term perspectives of CRESST are discussed.Comment: 12 pages, 6 figure

    OPENING ADDRESS: THE IMPORTANCE OF WILDLIFE DAMAGE CONTROL IN TEXAS

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    Let me first indicate that I have been interested in wildlife damage control programs for a good part of my life. My first experience, at the tender age of 6 years, was hard to accept when coyotes killed my 4-H pig. The importance of wildlife damage control has been clear to me since that time. Unfortunately, the importance of control is not often clear to those people who have not directly experienced wildlife damage

    Expression analysis of <em>lrrk1</em>, <em>lrrk2</em> and <em>lrrk2</em> splice variants in mice.

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    Missense mutations in the leucine-rich repeat kinase 2 gene (LRRK2) are linked to autosomal dominant forms of Parkinson&#39;s disease (PD). In order to get insights into the physiological role of Lrrk2, we examined the distribution of Lrrk2 mRNA and different splice variants in the developing murine embryo and the adult brain of Mus musculus. To analyse if the Lrrk2-paralog, Lrrk1, may have redundant functions in PD-development, we also compared Lrrk1 and Lrrk2 expression in the same tissues. Using radioactive in situ hybridization, we found ubiquitous expression of both genes at low level from embryonic stage E9.5 onward, which progressively increased up until birth. The developing central nervous system (CNS) displayed no prominent Lrrk2 mRNA signals at these time-points. However, in the entire postnatal brain Lrrk2 became detectable, showing strongest level in the striatum and the cortex of adult mice; Lrrk1 was only detectable in the mitral cell layer of the olfactory bulb. Thus, due to the non-overlapping expression patterns, a redundant function of Lrrk2 and Lrrk1 in the pathogenesis of PD seems to be unlikely. Quantification of Lrrk2 mRNA and protein level in several brain regions by real-time PCR and Western blot verified the striatum and cortex as hotspots of postnatal Lrrk2 expression. Strong expression of Lrrk2 is mainly found in neurons, specifically in the dopamine receptor 1 (DRD1a) and 2 (DRD2)-positive subpopulations of the striatal medium spiny neurons. Finally, we identified 2 new splice-variants of Lrrk2 in RNA-samples from various adult brain regions and organs: a variant with a skipped exon 5 and a truncated variant terminating in an alternative exon 42a. In order to identify the origin of these two splice variants, we also analysed primary neural cultures independently and found cell-specific expression patterns for these variants in microglia and astrocytes

    The CRESST dark matter search

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    The CRESST (Cryogenic Rare Event Search with Superconducting Thermometers) experiment at the Gran Sasso Laboratory will search for dark matter WIMPs using cryogenic detectors. In the first stage we will use four 262 g sapphire crystals with thresholds of about 0.5 keV. This low threshold gives us sensitivity to WIMP masses below 10 GeV, making CRESST complementary to other dark matter searches. The main installation in Gran Sasso is now complete and we report on the first detector tests

    Pink1-deficiency in mice impairs gait, olfaction and serotonergic innervation of the olfactory bulb

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    Parkinson's Disease (PD) is the most common neurodegenerative movement disorder. Autosomal-recessive mutations in the mitochondrial protein kinase PINK1 (PTEN-induced kinase 1) account for 1-2% of the hereditary early-onset cases. To study the mechanisms underlying disease development, we generated Pink1-deficient mice. In analogy to other genetic loss-of-function mouse models, Pink1(-/-) mice did not show morphological alterations in the dopaminergic system. As a consequence, no gross motor dysfunctions were observed indicating that these mice do not develop the cardinal symptoms of PD. Nonetheless, symptoms which develop mainly before bradykinesia, rigidity and resting tremor were clearly evident in Pink1-deficient mice. These symptoms were gait alterations and olfactory dysfunctions. Remarkably in the glomerular layer of the olfactory bulb the density of serotonergic fibers was significantly reduced. Concerning mitochondrial morphology, neurons in Pink1(-/-) mice had less fragmented mitochondria. In contrast, upon acute knock-down of Pink1 increased mitochondrial fragmentation was observed in neuronal cultures. This fragmentation was, however, evened out within days. Taken together, we demonstrate that Pink1-deficient mice exhibit behavioral symptoms of early phases of PD and present systematic experimental evidence for compensation of Pink1-deficiency at the cellular level. Thus, Pink1-deficient mice represent a model for the early phases of PD in which compensation may still impede the onset of neurodegeneration. Consequently, these mice are a valuable tool for studying Pink1-related PD development, as well as for searching for reliable PD biomarkers
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