The Siberian chipmunk is the only species that is found outside of North America - its range extends throughout northern Asia, from central Russia to Japan. Western chipmunks inhabit the western states as well as most of Canada. As indicated by its name, the eastern chipmunk inhabits most of the eastern half of the United States and Canada. Identifying Features: Shades of brown/yellow/grey fur with white and black stripes down the backĪll species of chipmunks are native to North America, except one - the Siberian chipmunk.Average Lifespan in the Wild: 2-3 years.Average Size: 2-6" long with a 3" tail less than 1 lb.Neotamias (mostly western chipmunks - 23 existing species).
#Chipmunk facies full
Implications for genetic counseling.Shop Chipmunk Solutions » view Full Pest Library » It may be mistaken for iron deficiency: excluded by measurement of serum iron, total iron-bindingĢ. Why it is important to recognize β-thalassemia minor /traitġ. Hypochromia, microcytosis, basophilic stippling, and target cells in peripheral smear along witn increase in HbA2 in Hemoglobin electrophoresis Hematopoietic stem cell transplantation – curative! Iron chelation therapy if there is iron overload Radiology – Bony features as described earlier! HbA2 levels are sometimes high but more often are normal or low. Peripheral smear- Marked anisopoikilocytosis, Microcytic hypochromic with many target cells. Hair–on end appearance/ Crew cut appearance – Suggests an extreme degree of medullary erythropoiesis and show long, thin vertical striations that resemble hairs standing on ends on x rays.ĬBC- Markedly decreased hemoglobin, Low MCV & MCH manifest with Pallor, splenomegaly, fever & failure to thrive along with skeletal deformities ( classical thalassemis /chipmunk facies)Ĭhipmunk facies: Malocclusion due to overgrowth of maxilla with Prominent zygomatic bones and depression of nasal bridge, Frontal and posterior bossing and Large deformed skull Β-thalassemia intermedia – Independently of the genotype!Does not require transfusion or only sporadic transfusionsĪlso referred to as Mediterranean Anemia and Cooley’s anemia where Anemia usually appear in first year of life at the time when gamma chains are not replaced by beta chains. Β-thalassemia minor /trait – Heterozygotes with one β-thalassemia gene and one normal gene (β+/β or β0/β) with mild asymptomatic microcytic anemia.
– individuals with two β-thalassemia alleles (β+/β+, β+/β0, or β0/β0) with severe, transfusion-dependent anemia
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The main mechanism is Impaired β globin chain synthesis and consequent relative excess of α chains leading to anemia, hepatosplenomegaly, skeletal deformities and secondary hemochromatosis as illustrated below. Mutations affecting mRNA translation – Chain terminator mutations.they can be either Nonsense mutation or Frameshift mutations, which finally Block translation, thereby Prevent beta globin synthesis and hence these are βo mutations These reduce transcription by 75 to 80%, Some normal beta globin Chains are made and hence these are β+ mutationsģ. Transcription mutations – Promotor region mutations Some destroy normal mRNA splicing junctions which Completely prevent the production of betaglobin mRNA synthesis ,leading to βo mutationsĢ. Hence Some normal beta globin mRNA is also made and thereby these are β+ mutationsī. Create an “ectopic” splice within an intron leading to Both normal and abnormal splicing. Mutations affecting mRNA processing – Splicing mutationsĪ. Β+ mutations – reduced (but detectable) β-globin synthesisġ. Majority of the mutations are point mutations. Hemolytic anemia due to deficient synthesis of β globin chains.
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