24 results on '"Jäderlund, Karin Hultin"'
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2. Assessment of glial fibrillary acidic protein and anti-glial fibrillary acidic protein autoantibody concentrations and necrotising meningoencephalitis risk genotype in dogs with pug dog myelopathy.
- Author
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Rohdin, Cecilia, Ljungvall, Ingrid, Jäderlund, Karin Hultin, Svensson, Anna, Lindblad-Toh, Kerstin, and Häggström, Jens
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- 2024
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3. Granulomatous interstitial polymyositis and intramuscular neuritis in a dog
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Hultman, Josefin, Rosati, Marco, Grøn, Tone Kristensen, Matiasek, Kaspar, Trangerud, Cathrine, and Jäderlund, Karin Hultin
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- 2021
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4. Mutations in the CYP27B1 gene cause vitamin D dependent rickets in pugs
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Rohdin, Cecilia, primary, Wang, Chao, additional, Brander, Gustaf, additional, Rondahl, Veronica, additional, Karlsson, Åsa, additional, Friling, Lisa, additional, Fischetti, Anthony, additional, Meadows, Jennifer, additional, Häggström, Jens, additional, Jäderlund, Karin Hultin, additional, Ljungvall, Ingrid, additional, and Lindblad‐Toh, Kerstin, additional
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- 2023
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5. 42 - Bornavirus Infection
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Wensman, Jonas Johansson, Berg, Mikael, and Jäderlund, Karin Hultin
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- 2023
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6. Borna disease virus infection in cats
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Wensman, Jonas Johansson, Jäderlund, Karin Hultin, Holst, Bodil Ström, and Berg, Mikael
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- 2014
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7. Validation of the diagnosis canine epilepsy in a Swedish animal insurance database against practice records
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Heske, Linda, Berendt, Mette, Jäderlund, Karin Hultin, Egenvall, Agneta, and Nødtvedt, Ane
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- 2014
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8. A 1 bp deletion in HACE1 causes ataxia in Norwegian elkhound, black
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Bellamy, Kim K. L., primary, Skedsmo, Fredrik S., additional, Hultman, Josefin, additional, Arnet, Ellen F., additional, Guttersrud, Ole Albert, additional, Skogmo, Hege Kippenes, additional, Thoresen, Stein Istre, additional, Espenes, Arild, additional, Jäderlund, Karin Hultin, additional, and Lingaas, Frode, additional
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- 2022
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9. List of Contributors
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Acke, Els, Adolph, Christopher B., Afonso, Maria, Allen, Kelly E., Arzi, Boaz, Balsa, Ingrid, Baneth, Gad, Barber, Renee, Barker, Emi N., Barrs, Vanessa R., Beatty, Julia A., Berg, Mikael, Birkenheuer, Adam J., Blagburn, Byron L., Bond, Ross, Bowman, Dwight D., Breitschwerdt, Edward B., Buonavoglia, Canio, Burgess, Brandy A., Burkitt Creedon, Jamie M., Byrne, Barbara A., Casal, Margret L., Chalker, Victoria J., Chomel, Bruno B., Cohn, Leah A., Cole, Lynette K., Cole, Stephen D., Conboy, Gary A., Cortinas, Roberto, Coyner, Kimberly, Culp, William T.N., Daniels, Joshua B., Davidson, Autumn P., Dear, Jonathan D., Decaro, Nicola, DeClue, Amy E., Diaz-Campos, Dubraska, Diniz, Pedro Paulo V.P., Dubey, Jitender P., Dubovi, Edward J., Eckstrand, Chrissy, Ellis, John A., Elsemore, David A., Epstein, Steven E., Evermann, James F., Foley, Janet E., Giger, Urs, Goldstein, Ellie J.C., Granick, Jennifer, Gremião, Isabella D.F., Grooters, Amy M., Gunn-Moore, Danièlle A., Guptill, Lynn, Hamer, Sarah A., Harrus, Shimon, Hartmann, Katrin, Henke, Diana, Hodzic, Emir, Hofmann-Lehmann, Regina, Howerth, Elizabeth W., Jäderlund, Karin Hultin, Hurley, Kate F., Jacobson, Linda S., Wensman, Jonas Johansson, Kapatkin, Amy S., Kent, Marc, Ketzis, Jennifer K., Kidd, Linda, Kraus, Stacy, Krockenberger, Mark, Lappin, Michael R., Lee, Alice C.Y., Lee-Fowler, Tekla, Little, Susan E., Littman, Meryl P., Lobetti, Remo, Lucio-Forster, Araceli, Luff, Jennifer A., Lutz, Hans, Marcondes, Mary, Marks, Stanley L., Marsilio, Sina, McDonough, Patrick L., Menezes, Rodrigo C., Merkel, Lindsay, Mills, W. Zach, Miranda, Luisa H.M., Moore, George E., Moriello, Karen A., Mourning, Alyssa C., Munday, John S., Mylonakis, Mathios E., Nagamori, Yoko, Nelson, C. Thomas, Nordstoga, Anne B., Norris, Jacqueline M., O’Brien, Carolyn R., O’Halloran, Conor, Otto, Cynthia M., Papich, Mark G., Parrish, Colin R., Pedersen, Niels C., Peregrine, Andrew S., Pereira, Sandro A., Petersen, Christine, Prescott, John F., Priestnall, Simon L., Qurollo, Barbara, Radford, Alan, Rankin, Shelley C., Reagan, Krystle L., Reichard, Mason V., Reinero, Carol, Saleh, Meriam N., Sapp, Sarah G.H., Saunders, Ashley B., Schubach, Tânia M.P., Schuller, Simone, Scorza, Valeria, Sellon, Rance K., Sharp, Claire R., Silverstein, Deborah, Singh, Ameet, Sinnott-Stutzman, Virginia, Snowden, Karen F., Solano-Gallego, Laia, Spindel, Miranda, Starkey, Lindsay A., Stern, Joshua A., Stiles, Jean, Straubinger, Reinhard K., Stull, Jason W., Sykes, Jane E., Tasker, Séverine, Thomas, Jennifer E., Thomasy, Sara M., Tipold, Andrea, Tolbert, M. Katherine, Vahlenkamp, Thomas W., Vandevelde, Marc, Vincent-Johnson, Nancy, Vishkautsan, Polina, Waner, Trevor, Weese, J. Scott, Westropp, Jodi L., White, Stephen D., Winston, Jenessa A., Wulcan, Judit M., and Yabsley, Michael J.
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- 2023
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10. Thoracolumbar meningeal fibrosis in pugs
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Rohdin, Cecilia, primary, Ljungvall, Ingrid, additional, Häggström, Jens, additional, Leijon, Alexandra, additional, Lindblad‐Toh, Kerstin, additional, Matiasek, Kaspar, additional, Rosati, Marco, additional, Wohlsein, Peter, additional, and Jäderlund, Karin Hultin, additional
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- 2020
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11. Re-emergence of hereditary polyneuropathy in Scandinavian Alaskan malamute dogs—old enemy or new entity? A case series
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Jäderlund, Karin Hultin, Rohdin, Cecilia, Berendt, Mette, Stigen, Øyvind, Fredholm, Merete, Espenes, Arild, Bjerkås, Inge, and Moe, Lars
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Inherited ,lcsh:Veterinary medicine ,Intracellular Signaling Peptides and Proteins ,Cell Cycle Proteins ,NDRG1-gene ,Brief Communication ,Pedigree ,Polyneuropathies ,Dogs ,Gene Expression Regulation ,Polyneuropathy ,Mutation ,Dog ,Animals ,Recessive ,lcsh:SF600-1100 ,Genetic Predisposition to Disease ,Dog Diseases - Abstract
A homozygous mutation has been identified in the N-myc downstream-regulated gene 1 (NDRG1) in recent cases of polyneuropathy in Alaskan malamute dogs from the Nordic countries and USA. The objective of the present study was to determine if cases diagnosed 30–40 years ago with polyneuropathy in the Alaskan malamute breed in Norway had the same hereditary disease as the recent cases. Fourteen historical cases and 12 recently diagnosed Alaskan malamute dogs with hereditary polyneuropathy, and their parents and littermates (n = 88) were included in this study (total n = 114). After phenotyping of historical and recent cases, NDRG1 genotyping was performed using DNA extracted from archived material from five Norwegian dogs affected by the disease in the late 1970s and 1980s. In addition, pedigrees were analysed. Our study concluded that historical and recent phenotypic polyneuropathy cases were carrying the same NDRG1-mutation. The pedigree analysis showed that all affected Alaskan malamute cases with polyneuropathy could be traced back to one common ancestor of North American origin. By this study, a well-documented example of the silent transmission of recessive disease-causing alleles through many generations is provided, demonstrated by the re-emergence of a phenotypically and genetically uniform entity in the Scandinavian Alaskan malamute population.
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- 2017
12. High prevalence of gait abnormalities in pugs
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Rohdin, Cecilia, primary, Jäderlund, Karin Hultin, additional, Ljungvall, Ingrid, additional, Lindblad-Toh, Kerstin, additional, and Häggström, Jens, additional
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- 2018
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13. Basal Autophagy Is Altered in Lagotto Romagnolo Dogs with an ATG4D Mutation
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Syrjä, Pernilla, primary, Anwar, Tahira, additional, Jokinen, Tarja, additional, Kyöstilä, Kaisa, additional, Jäderlund, Karin Hultin, additional, Cozzi, Francesca, additional, Rohdin, Cecilia, additional, Hahn, Kerstin, additional, Wohlsein, Peter, additional, Baumgärtner, Wolfgang, additional, Henke, Diana, additional, Oevermann, Anna, additional, Sukura, Antti, additional, Leeb, Tosso, additional, Lohi, Hannes, additional, and Eskelinen, Eeva-Liisa, additional
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- 2017
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14. TECPR2 Associated Neuroaxonal Dystrophy in Spanish Water Dogs
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Hahn, Kerstin, primary, Rohdin, Cecilia, additional, Jagannathan, Vidhya, additional, Wohlsein, Peter, additional, Baumgärtner, Wolfgang, additional, Seehusen, Frauke, additional, Spitzbarth, Ingo, additional, Grandon, Rodrigo, additional, Drögemüller, Cord, additional, and Jäderlund, Karin Hultin, additional
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- 2015
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15. Clinical characteristics of epilepsy of unknown origin in the Rottweiler breed
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Heske, Linda, primary, Körberg, Izabella Baranowska, additional, Nødtvedt, Ane, additional, and Jäderlund, Karin Hultin, additional
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- 2015
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16. A KCNJ10 mutation previously identified in the Russell group of terriers also occurs in Smooth-Haired Fox Terriers with hereditary ataxia and in related breeds
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Rohdin, Cecilia, primary, Gilliam, Douglas, additional, O’Leary, Caroline A., additional, O’Brien, Dennis P., additional, Coates, Joan R., additional, Johnson, Gary S., additional, and Jäderlund, Karin Hultin, additional
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- 2015
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17. Expression of interferon gamma in the brain of cats with natural Borna disease virus infection
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Wensman, Jonas Johansson, Ilbäck, Carolina, Hjertström, Elina, Blomström, Anne-Lie, Gustavsson, Malin Hagberg, Jäderlund, Karin Hultin, Ström-Holst, Bodil, Belák, Sándor, Berg, Anna-Lena, and Berg, Mikael
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- 2011
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18. Acquired motor neuron loss causing severe pelvic limb contractures in a young cat
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Rohdin, Cecilia, Karlstam, Erika, Jäderlund, Karin Hultin, and Shelton, G. Diane
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- 2010
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19. Sensory Ataxic Neuropathy in Golden Retriever Dogs Is Caused by a Deletion in the Mitochondrial tRNATyr Gene
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Baranowska, Izabella, primary, Jäderlund, Karin Hultin, additional, Nennesmo, Inger, additional, Holmqvist, Erik, additional, Heidrich, Nadja, additional, Larsson, Nils-Göran, additional, Andersson, Göran, additional, Wagner, E. Gerhart H., additional, Hedhammar, Åke, additional, Wibom, Rolf, additional, and Andersson, Leif, additional
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- 2009
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20. A Deletion in the N-Myc Downstream Regulated Gene 1 (NDRG1) Gene in Greyhounds with Polyneuropathy.
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Drögemüller, Cord, Becker, Doreen, Kessler, Barbara, Kemter, Elisabeth, Tetens, Jens, Jurina, Konrad, Jäderlund, Karin Hultin, Flagstad, Annette, Perloski, Michele, Lindblad-Toh, Kerstin, and Matiasek, Kaspar
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POLYNEUROPATHIES ,PERIPHERAL neuropathy ,GREYHOUNDS ,DOG diseases ,GENETIC mutation ,VETERINARY therapeutics ,VETERINARY medicine ,PHYSIOLOGY ,THERAPEUTICS - Abstract
The polyneuropathy of juvenile Greyhound show dogs shows clinical similarities to the genetically heterogeneous Charcot- Marie-Tooth (CMT) disease in humans. The pedigrees containing affected dogs suggest monogenic autosomal recessive inheritance and all affected dogs trace back to a single male. Here, we studied the neuropathology of this disease and identified a candidate causative mutation. Peripheral nerve biopsies from affected dogs were examined using semi-thin histology, nerve fibre teasing and electron microscopy. A severe chronic progressive mixed polyneuropathy was observed. Seven affected and 17 related control dogs were genotyped on the 50k canine SNP chip. This allowed us to localize the causative mutation to a 19.5 Mb interval on chromosome 13 by homozygosity mapping. The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D). Therefore, we considered NDRG1 a positional and functional candidate gene and performed mutation analysis in affected and control Greyhounds. A 10 bp deletion in canine NDRG1 exon 15 (c.1080_1089delTCGCCTGGAC) was perfectly associated with the polyneuropathy phenotype of Greyhound show dogs. The deletion causes a frame shift (p.Arg361SerfsX60) which alters several amino acids before a stop codon is encountered. A reduced level of NDRG1 transcript could be detected by RT-PCR. Western blot analysis demonstrated an absence of NDRG1 protein in peripheral nerve biopsy of an affected Greyhound. We thus have identified a candidate causative mutation for polyneuropathy in Greyhounds and identified the first genetically characterized canine CMT model which offers an opportunity to gain further insights into the pathobiology and therapy of human NDRG1 associated CMT disease. Selection against this mutation can now be used to eliminate polyneuropathy from Greyhound show dogs. [ABSTRACT FROM AUTHOR]
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- 2010
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21. Sensory Ataxic Neuropathy in Golden Retriever Dogs Is Caused by a Deletion in the Mitochondrial tRNATyrGene.
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Baranowska, Izabella, Jäderlund, Karin Hultin, Nennesmo, Inger, Holmqvist, Erik, Heidrich, Nadja, Larsson, Nils-Göran, Andersson, Göran, Wagner, E. Gerhart H., Hedhammar, Åke, Wibom, Rolf, and Andersson, Leif
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GOLDEN retriever , *TRANSFER RNA , *OLIGONUCLEOTIDES , *GENETIC polymorphism research , *DOG diseases , *GENETICS - Abstract
Sensory ataxic neuropathy (SAN) is a recently identified neurological disorder in golden retrievers. Pedigree analysis revealed that all affected dogs belong to one maternal lineage, and a statistical analysis showed that the disorder has a mitochondrial origin. A one base pair deletion in the mitochondrial tRNATyr gene was identified at position 5304 in affected dogs after re-sequencing the complete mitochondrial genome of seven individuals. The deletion was not found among dogs representing 18 different breeds or in six wolves, ruling out this as a common polymorphism. The mutation could be traced back to a common ancestor of all affected dogs that lived in the 1970s. We used a quantitative oligonucleotide ligation assay to establish the degree of heteroplasmy in blood and tissue samples from affected dogs and controls. Affected dogs and their first to fourth degree relatives had 0-11% wild-type (wt) sequence, while more distant relatives ranged between 5% and 60% wt sequence and all unrelated golden retrievers had 100% wt sequence. Northern blot analysis showed that tRNATyr had a 10-fold lower steady-state level in affected dogs compared with controls. Four out of five affected dogs showed decreases in mitochondrial ATP production rates and respiratory chain enzyme activities together with morphological alterations in muscle tissue, resembling the changes reported in human mitochondrial pathology. Altogether, these results provide conclusive evidence that the deletion in the mitochondrial tRNATyr gene is the causative mutation for SAN. [ABSTRACT FROM AUTHOR]
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- 2009
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22. ELECTRIC STIMULATION OF A TRANSSECTED NERVE DOES NOT SEEM TO PREVENT LOSS OF SENSORY NEURONS: AN EXPERIMENTAL STUDY IN CATS.
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Liss, Anders G., Lagerström, Anne, Jäderlund, Karin Hultin, Bowald, Staffan, Ekenstam, Fredrik W. af, Flink, Roland, and Wiberg, Mikael
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ELECTRIC stimulation ,SENSORY neurons ,NERVOUS system injuries - Abstract
Injury to a sensory nerve often results in a clinically poor long term outcome, possibly as a result of the extensive loss of neurons within the dorsal root ganglia (DRG), which has been shown in several experimental studies. This loss is possibly caused by interruption of the sensory input and axonal transport in the damaged afferent nerve. To investigate the importance of sensory afferent input into a nerve a pulsed electric stimulation was applied on the proximal part of the superficial radial nerve after transsection and microsurgical repair. The purpose was to simulate nerve impulses and thereby mask the severity of the injury. To test this hypothesis a pilot study was undertaken in eight cats. The neuronal tracer showed that the median neuronal loss was 38% of the neurons of the dorsal root ganglia that received afferents from the nerve investigated, which corresponds to the figure in a previous study in which electric stimulation was not used. Artificial sensory stimulation during regeneration in a transsected and repaired peripheral nerve therefore does not seem to reduce neuronal loss. [ABSTRACT FROM AUTHOR]
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- 1999
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23. NDRG1 og PrPC i perifert myelinvedlikehold : innsikt fra morfologiske studier i to unike dyremodeller
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Skedsmo, Fredrik Strebel, Jäderlund, Karin Hultin, Espenes, Arild, and Tranulis, Michael A.
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Charcot-Marie-Tooth ,Dogs ,nervous system ,NDRG1 ,Myelin ,Polyneuropathy ,Goats ,Alaskan Malamute ,PrPC ,Cellular prion protein ,Demyelination ,N-myc downstream-regulated gene 1 - Abstract
Peripheral nerves transmit signals between peripheral tissue and the central nervous system, essential for normal motor and sensory function. To enable this, the integrity of both the axon and Schwann cell is crucial. The Schwann cell forms a myelin sheath around large diameter axons, necessary for rapid nerve conduction and axonal survival. Neuropathies, diseases affecting peripheral nerves, have diverse etiologies and may cause severe clinical signs in both human and animals. Some neuropathies are caused by inherited deficiencies in proteins necessary for normal axonal function or formation/maintenance of the myelin sheath. In this work, we have investigated how deficiencies in NDRG1 or PrPC affect peripheral nerve myelin maintenance by using morphological studies in two unique, spontaneous animal models. The hereditary polyneuropathy of Alaskan Malamutes is associated with a mutation in N-myc downstream-regulated gene 1 (NDRG1). Other mutations in the same gene cause polyneuropathies in humans, rodent models and Greyhound show dogs. However, the function of NDRG1 in peripheral nerves is largely unknown and the pathomorphological changes described in NDRG1-associated neuropathies of different species diverge. Whereas the human disease, denominated Charcot-Marie-Tooth disease type 4D, is considered a primary demyelinating disease with secondary axonal loss, axonal degeneration dominated in the polyneuropathy of Greyhounds. A detailed mapping of NDRG1 in canine tissues and cells presented in this thesis revealed high NDRG1 expression in epithelia and myelinating Schwann cells. A phosphorylated isoform of the protein localized to the centrosomes and cleavage furrow in a primary canine Schwann cell culture. Phosphorylated NDRG1 was restricted to the abaxonal cytoplasm of myelinating Schwann cells in control dogs, but this signal was not observed in an affected Alaskan Malamute. Ultrastructural studies and teased fiber preparations of nerves from neuropathic Alaskan Malamutes uncovered a demyelinating neuropathy associated with accumulation of actin in the Schwann cell and prominent myelin infoldings. The latter ultimately segregated the axon into pockets with aggregates of organelles, suggestive of early axonal degeneration. We therefore suggest that impaired NDRG1 function in the myelinating Schwann cells of affected Alaskan Malamutes results in deranged myelin maintenance, demyelination and secondary axonal degeneration. The cellular prion protein (PrPC) has been studied extensively because of its role in the development of transmissible spongiform encephalopathies in several species, such as Creutzfeldt-Jakobs disease in humans, bovine spongiform encephalopathy (“mad cow disease”) in cattle and scrapie in small ruminants. In these diseases, a misfolded isoform of the protein, PrPSc, accumulates in the brain and ultimately results in neuronal death. The normal functions of PrPC are not fully understood. Some of the phenotypes reported from transgenic mice lacking PrPC have later been ascribed to other genes, but recent reports have suggested that PrPC is important in dampening pro-inflammatory signaling and in myelin maintenance. We have used a nontransgenic, spontaneous model to investigate the latter; a line of Norwegian dairy goats lacking PrPC. Morphological studies revealed a demyelinating neuropathy with infiltration of macrophages and lymphocytes, vacuolated fibers and paranodal myelin outfoldings. Peripheral nerve lipid composition of adult goats lacking PrPC was significantly different from controls, while no difference was observed in young goats, suggesting a progressive disease. In conclusion, this is the first report of a demyelinating polyneuropathy caused by loss of PrPC in a nontransgenic mammal, supporting that PrPC has a vital role in peripheral nerve myelin maintenance. Perifere nerver overfører nerveimpulser mellom perifert vev og sentralnervesystemet, og er derfor essensielle for normal motorisk og sensorisk funksjon. For opprettholdelse av denne funksjonen, er både aksonet og den Schwannske cellen viktige. Aksonet er en utløper fra nervecellen og sørger for overføring av nerveimpulser. Den Schwannske cellen danner en myelinskjede rundt større aksoner. Dette er nødvendig for rask nerveledningshastighet og aksonal overlevelse. Nevropatier, sykdommer i perifere nerver, har ulik etiologi og kan forårsake alvorlige kliniske tegn både hos mennesker og dyr. Noen nevropatier er forårsaket av arvelige forstyrrelser i proteiner som er nødvendig for normal aksonal funksjon eller dannelse/vedlikehold av myelinskjeden. I dette arbeidet har vi undersøkt hvordan mangel på NDRG1 eller PrPC påvirker myelinvedlikehold i perifere nerver ved å bruke morfologiske studier i to unike, spontane dyremodeller. Arvelig polynevropati hos alaskan malamute er assosiert med en mutasjon i N-myc downstream-regulated gene 1 (NDRG1). Andre mutasjoner i samme genet forårsaker polynevropatier hos menneske, gnagermodeller og utstillingslinjer av greyhound. Funksjonen til NDRG1 i perifere nerver er imidlertid ukjent, og de patomorfologiske forandringene ved NDRG1-assosierte nevropatier hos ulike arter divergerer. Mens den humane nevropatien, Charcot-Marie-Tooths sykdom type 4D, er ansett for å være en primær demyeliniserende sykdom med sekundært aksonalt tap, dominerte aksonal degenerasjon ved polynevropati hos greyhound. En detaljert kartlegging av NDRG1 i celler og vev fra hund presentert i denne avhandlingen viser høye nivåer av NDRG1 i epitel og myeliniserende Schwannske celler. En fosforylert isoform av proteinet ble lokalisert i centrosomer og kløyvingsfuren hos Schwannske celler isolert fra hund. Fosforylert NDRG1 var begrenset til abaksonale cytoplasma i myeliniserende Schwannske celler i kontrollhunder, men dette signalet ble ikke observert i en syk alaskan malamute. Ultrastrukturelle studier og teased nerve fibers av nerver fra affiserte alaskan malamuter avslørte en demyeliniserende nevropati assosiert med aktinaggregater i de myeliniserende Schwannske cellene og uttalte innfoldinger av myelin. Innfoldingene delte stedvis aksonene inn i atskilte lommer med aggregater av organeller, forenelig med tidlig aksonal degenerasjon. Resultatene tyder på at svekket NDRG1-funksjon i myeliniserende Schwannske celler hos affiserte alaskan malamuter fører til forstyrret vedlikehold av myelin, demyelinisering og sekundær aksonal degenerasjon. Det cellulære prionproteinet (PrPC) har blitt grundig studert på grunn av sin rolle i utvikling av overførbare spongiforme encefalopatier, eller prionsykdommer, hos flere arter, for eksempel Creutzfeldt-Jakobs sykdom hos menneske, bovin spongiform encefalopati («kugalskap») hos storfe og skrapesjuke hos små drøvtyggere. Ved disse sykdommene vil en misfoldet isoform av proteinet, PrPSc, akkumulere i hjernen og tilslutt resultere i nevronal celledød. Normalfunksjonen til PrPC er ikke fullstendig forstått, og forståelsen av denne kan være viktig for å belyse den molekylære patogenesen ved prionsykdommer. Noen fenotyper rapportert fra transgene mus uten PrPC ble senere vist å skyldes andre gener, men nylige rapporter foreslår at PrPC er viktig for å dempe proinflammatorisk signalering og myelinvedlikehold. Vi har brukt en ny, ikke-transgen, spontan modell - en linje av norske melkegeiter som mangler PrPC - til å undersøke om denne modellen kan bekrefte tidligere studier fra transgene mus som har vist myelinskader. Morfologiske studier hos geiter uten PrPC avslørte en demyeliniserende nevropati med infiltrasjon av makrofager og lymfocytter, vakuoliserte nervefibre og paranodale myelinutfoldinger. Lipidsammensetningen i perifere nerver hos voksne geiter uten PrPC var signifikant forskjellig fra kontrollene, mens ingen forskjell ble observert hos unge dyr, noe som tyder på en progredierende sykdom. Dette er den første rapporten av en demyeliniserende polynevropati forårsaket av PrPC-mangel hos et ikke-transgent pattedyr, og støtter at PrPC har en viktig rolle i myelinvedlikehold.
- Published
- 2020
24. Cerebral ventricular size in developing normal kittens measured by ultrasonography.
- Author
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Jäderlund KH, Hansson K, Berg AL, Sjöström A, and Narfström K
- Subjects
- Animals, Cerebral Ventricles diagnostic imaging, Female, Male, Reference Values, Ultrasonography veterinary, Cats anatomy & histology, Cats growth & development, Cerebral Ventricles anatomy & histology, Cerebral Ventricles growth & development
- Abstract
To evaluate the age of fontanelle closure of normal kittens and the size of their lateral ventricles, 50 ultrasonographic examinations using the bregmatic fontanelle as an acoustic window were made. Seven kittens, laboratory animals, were included in the study. To verify the location of the lateral ventricle, two of the kittens were sacrificed as neonates. In one of them ink was injected prior to autopsy into one lateral ventricle under sonographic guidance. In a longitudinal study of five of the kittens, the skull depth and the depth of the central part of the lateral ventricle reproduced in a longitudinal view could be measured up to the age of about 5 months. During that period, the skull depth increased from a median value of 1.95 cm (1.92-1.98) in a seven-day-old cat to 2.58 cm (2.52-2.59) in a 154-day-old cat, while the afore-mentioned ventricle values increased from 0.3 mm to 1.1 mm.
- Published
- 2003
- Full Text
- View/download PDF
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