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Ridpath, Julia F,Falkenberg, Shollie M,Bauermann, Fernando V,VanderLey, Brian L,Do, YoonJung,Flores, Eduardo F,Rodman, Dianne M,Neill, John D American Veterinary Medical Association 2013 American journal of veterinary research Vol.74 No.3
<P>To compare acute infection of cattle exposed to a high-virulence (HV) bovine viral diarrhea virus (BVDV), low-virulence (LV) BVDV, or HoBi-like virus.</P>
Daniel Kondziella,Siska Frahm-Falkenberg 대한신경과학회 2011 Journal of Clinical Neurology Vol.7 No.2
Anton’s syndrome is arguably the most striking form of anosognosia. Patients with this syndrome behave as if they can see despite their obvious blindness. Although best known for his description of asomatognosia and visual anosognosia, Gabriel Anton (1858-1933) made other significant contributions to the clinical neurosciences, including pioneering work in neurosurgery, neuropsychology, and child psychiatry. However, it has not been recognized in the English literature that Anton was also a dedicated advocate of eugenics and racial hygiene. This paper provides a case of Anton’s syndrome and puts the works of Gabriel Anton into their historic context.
Comparison of the Digestibility of Grain and Forage by Sheep, Red and Fallow Deer
Ru, Y.J.,Glatz, P.C.,Miao, Z.H.,Swanson, K.,Falkenberg, S.,Wyatt, S. Asian Australasian Association of Animal Productio 2002 Animal Bioscience Vol.15 No.6
Two experiments were conducted to compare digestibility of 12 diets in sheep, red and fallow deer. No differences (p>0.05) between sheep, red and fallow deer in digestibility of dry matter, organic matter and digestible energy content for all diets were found except for the sorghum diet and medic hay. Sheep and fallow deer digested the sorghum diet better than red deer. An in vitro study showed that sheep had a lower in vitro dry matter digestibility and digestible energy content than both red and fallow deer, with a significant interaction between animal species and feed ingredient. Deer digested straws and hays better (p<0.05) than sheep. In vitro digestibility was lower (p<0.05) than in vivo digestibility, but significantly correlated with in vivo digestibility for red and fallow deer. The in vitro method for digestibility estimation has potential as a rapid feed evaluation system for deer, but needs further validation.
Forage Intake and Nutrient Requirements of Fallow Weaner Deer in Southern Australia
Ru, Y.J.,Fischer, M.,Glatz, P.C.,Wyatt, S.,Swanson, K.,Falkenberg, S. Asian Australasian Association of Animal Productio 2003 Animal Bioscience Vol.16 No.5
Information on nutrient requirements and forage intake of fallow weaner deer is required for the development of feeding strategies during the year. An experiment was conducted in which 60 fallow weaner deer (grazing on medic and ryegrass based pastures) were supplemented with a concentrated diet at three levels. The diet contained 2% minerals, 30% lupin and 68% barley grain. Twelve deer from each treatment were dosed with commercial alkane capsules in May, June, July, September and October to predict nutrient intake. The relationships between body weight gain and intake of metabolisable energy and crude protein were established using a general linear models analysis. Dry matter intake from pastures ranged from 0.137 kg to 0.304 kg in May and June and increased to 1.2 kg in October. Nutrient intake from pastures was strongly influenced by amount of supplementary feed and gender. Digestible energy intake from pastures was 1.3, 3.8 and 6.1 MJ/day higher for males than females in July, August and October, respectively. The protein and energy intake was strongly correlated with body weight gain. The energy requirement for maintenance were 7.3, 8.2, 10.2, 10.2 and 10.7 MJ DE/day and the DE required for each kg body weight gain were 19, 18, 29, 34 and 49 MJ in May, June, August and October, respectively. The protein requirement for maintenance was 12.2, 12.6, 15.0, 11.4 and $8.5g/W^{0.75}$ in May, June, July, August and October, respectively. The nutrient requirement defined from this study can be used to assist farmers to explore the possible pasture and stock management practices under southern Australian conditions. However, further research is required to develop rapid and cheap methods for estimating dry matter intake, nutritive value of pastures and to quantify the potential growth rate of fallow deer in southern Australia.
Maintenance of respiratory chain function in mouse hearts with severely impaired mtDNA transcription
Freyer, Christoph,Park, Chan Bae,Ekstrand, Mats I.,Shi, Yonghong,Khvorostova, Julia,Wibom, Rolf,Falkenberg, Maria,Gustafsson, Claes M.,Larsson, Nils-Gö,ran Oxford University Press 2010 Nucleic acids research Vol.38 No.19
<P>The basal mitochondrial transcription machinery is essential for biogenesis of the respiratory chain and consists of mitochondrial RNA polymerase, mitochondrial transcription factor A (TFAM) and mitochondrial transcription factor B2. This triad of proteins is sufficient and necessary for mtDNA transcription initiation. Abolished mtDNA transcription caused by tissue-specific knockout of TFAM in the mouse heart leads to early onset of a severe mitochondrial cardiomyopathy with lethality within the first post-natal weeks. Here, we describe a mouse model expressing human TFAM instead of the endogenous mouse TFAM in heart. These rescue mice have severe reduction in mtDNA transcription initiation, but, surprisingly, are healthy at the age of 52 weeks with near-normal steady-state levels of transcripts. In addition, we demonstrate that heavy-strand mtDNA transcription normally terminates at the termination-associated sequence in the control region. This termination is abolished in rescue animals resulting in heavy (H)-strand transcription of the entire control region. In conclusion, we demonstrate here the existence of an unexpected mtDNA transcript stabilization mechanism that almost completely compensates for the severely reduced transcription initiation in rescue hearts. Future elucidation of the underlying molecular mechanism may provide a novel pathway to treat mitochondrial dysfunction in human pathology.</P>
Wilson, William C.,Hornig-Do, Hue-Tran,Bruni, Francesco,Chang, Jeong Ho,Jourdain, Alexis A.,Martinou, Jean-Claude,Falkenberg, Maria,Spå,hr, Henrik,Larsson, Nils-Gö,ran,Lewis, Richard J.,Hewit Oxford University Press 2014 Human Molecular Genetics Vol.23 No.23
<P>The p.N478D missense mutation in human mitochondrial poly(A) polymerase (mtPAP) has previously been implicated in a form of spastic ataxia with optic atrophy. In this study, we have investigated fibroblast cell lines established from family members. The homozygous mutation resulted in the loss of polyadenylation of all mitochondrial transcripts assessed; however, oligoadenylation was retained. Interestingly, this had differential effects on transcript stability that were dependent on the particular species of transcript. These changes were accompanied by a severe loss of oxidative phosphorylation complexes I and IV, and perturbation of <I>de novo</I> mitochondrial protein synthesis. Decreases in transcript polyadenylation and in respiratory chain complexes were effectively rescued by overexpression of wild-type mtPAP. Both mutated and wild-type mtPAP localized to the mitochondrial RNA-processing granules thereby eliminating mislocalization as a cause of defective polyadenylation. <I>In vitro</I> polyadenylation assays revealed severely compromised activity by the mutated protein, which generated only short oligo(A) extensions on RNA substrates, irrespective of RNA secondary structure. The addition of LRPPRC/SLIRP, a mitochondrial RNA-binding complex, enhanced activity of the wild-type mtPAP resulting in increased overall tail length. The LRPPRC/SLIRP effect although present was less marked with mutated mtPAP, independent of RNA secondary structure. We conclude that (i) the polymerase activity of mtPAP can be modulated by the presence of LRPPRC/SLIRP, (ii) N478D mtPAP mutation decreases polymerase activity and (iii) the alteration in poly(A) length is sufficient to cause dysregulation of post-transcriptional expression and the pathogenic lack of respiratory chain complexes.</P>
Terzioglu, M.,Ruzzenente, B.,Harmel, J.,Mourier, A.,Jemt, E.,Lopez, M.,Kukat, C.,Stewart, James B.,Wibom, R.,Meharg, C.,Habermann, B.,Falkenberg, M.,Gustafsson, Claes M.,Park, C.,Larsson, N.G. Cell Press 2013 Cell metabolism Vol.17 No.4
Mitochondrial transcription termination factor 1, MTERF1, has been reported to couple rRNA gene transcription initiation with termination and is therefore thought to be a key regulator of mammalian mitochondrial ribosome biogenesis. The prevailing model is based on a series of observations published over the last two decades, but no in vivo evidence exists to show that MTERF1 regulates transcription of the heavy-strand region of mtDNA containing the rRNA genes. Here, we demonstrate that knockout of Mterf1 in mice has no effect on mitochondrial rRNA levels or mitochondrial translation. Instead, loss of Mterf1 influences transcription initiation at the light-strand promoter, resulting in a decrease of de novo transcription manifested as reduced 7S RNA levels. Based on these observations, we suggest that MTERF1 does not regulate heavy-strand transcription, but rather acts to block transcription on the opposite strand of mtDNA to prevent transcription interference at the light-strand promoter.