Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0036474 (
scurvy
)
685
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The influences of chronic deficiency of L-ascorbic acid (AsA) on the differentiation of osteo-chondrogenic cells and the process of endochondral ossification were examined in the mandibular condyle and the tibial epiphysis and metaphysis by using Osteogenic Disorder Shionogi (ODS) rats that bear an inborn deficiency of L-gulonolactone oxidase. Weanling male rats were kept on an AsA-free diet for up to 4 weeks, until the symptoms of
scurvy
became evident. The tibiae and condylar processes of scorbutic rats displayed undersized and distorted profiles with thin cortical and scanty cancellous bones. In these scorbutic bones, the osteoblasts showed characteristic expanded round profiles of rough endoplasmic reticulum, and lay on the bone surface where the osteoid layer was missing. Trabeculae formation was deadlocked, although calcification of the cartilage matrix proceeded in both types of bone. Scorbutic condylar cartilage showed severe disorganization of cell zones, such as unusual thickening of the calcification zone, whereas the tibial cartilage showed no particular alterations (except for a moderately decreased population of chondrocytes). In condylar cartilage, hypertrophic chondrocytes were encased in a thickened calcification zone, and groups of nonhypertrophic chondrocytes occasionally formed cell nests surrounded by a metachromatic matrix in the hypertrophic cell zone. These results indicate that during endochondral ossification, chronic AsA deficiency depresses osteoblast function and disturbs the differentiation pathway of chondrocytes. The influence of
scurvy
on mandibular condyle cartilage is different from that on articular and epiphyseal cartilage of the tibia, suggesting that AsA plays different roles in endochondral ossification in the mandibular condyle and long bones.
Anat
Rec
2002 Oct 01
PMID:Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat. 1222 15
On the
Belgica
expedition (1897-1899), Dr F.A. Cook described a disease that he called 'polar anaemia' and on this expedition it affected most of the expedition members and caused one death. The symptoms were shortness of breath, abnormalities of the pulse and oedema (swelling of the legs) and the disease was clearly cardiac failure. During the heroic age of Antarctic exploration a similar disease affected at least eight other expeditions causing five other deaths. This disease was very similar (and probably identical) to a disease affecting (mostly) Scandinavian seamen and called 'ship beri-beri'. Both diseases were almost certainly what is now called wet beri-beri due to thiamine (vitamin B1) deficiency though most sufferers were probably also vitamin C deficient and some may have had both beri-beri and
scurvy
. It may have been exacerbated by invalid diets. This paper describes the disease and how it was considered and treated at the time.
Polar
Rec
(Gr Brit) 2012 Apr
PMID:'Polar anaemia': cardiac failure during the heroic age of Antarctic exploration. 2356 76