Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In nine sheep belonging to the same flock, C-cells hyperplasia of the thyroid, associated with calcinosis of the soft tissues is reported. The C-cells hyperplasia was probably due to excessive feeding with poultry waste, rich in calcium. The soft tissue mineralisation was a result of hypersecretion of calcitonin, a blood calcium-lowering hormone of the C-cells.
Vet Rec 1977 Oct 29
PMID:Enzootic calcinosis in sheep and C-cells hyperplasia of the thyroid. 61 71

The effects of magnesium deficiency in ovariectomized and estrogen-treated rats were examined in histological sections of bones and various soft tissues. The changes observed in the femora of intact rats deprived of magnesium for three weeks were: 1. a general increase in diaphyseal thickness, 2. the presence of localized fibrous or bony-like masses in subperiosteal and metaphyseal sites, and 3. the occurrence, although rare, of endosteal hyperplasia. In ovariectomized, magniesium-deprived animals, the incidence and location of fibrous masses were similar to that in the femora of magnesium-deficient intact rats; however, no increase in diaphyseal thickness was noted. Daily injections of 25 mug estradiol caused a reduction of the frequency of skeletal hyperplasia from 80% to 20%, as well as a reduction in femoral diaphyseal thickness. Estradiol hormone administration also brought about a marked alleviation of the dermal and neural manifestations of magnesium deficiency, but, at the same time, caused an exacerbation of renal calcinosis.
Anat Rec 1975 Nov
PMID:Skeletal effects of magnesium deficiency in normal, ovariectomized, and estrogen-treated rats. 120 Mar 32

Two young German shepherd dog littermates had progressive, painless, hindlimb ataxia. In both dogs plain radiography of the vertebral column revealed a solitary mineralised lesion on the dorsal laminae between the dorsal spines of the second and third thoracic vertebrae, and myelography with iopamidol demonstrated cord compression at the level of the lesions. The first dog died 18 hours after the myelography. A dorsal laminectomy performed in the second dog resulted in neurological improvement. A histopathological examination confirmed that both lesions were calcinosis circumscripta. The cause of the death of the first dog was meningitis.
Vet Rec 1992 Jun 27
PMID:Thoracic spinal calcinosis circumscripta causing cord compression in two German shepherd dog littermates. 149 70

Fibroblast growth factor-23 (FGF23) is a hormone that modulates circulating phosphate (P(i)) levels by controlling P(i) reabsorption from the kidneys. When FGF23 levels are deficient, as in tumoral calcinosis patients, hyperphosphatemia ensues. We show here in a murine model that Fgf23 ablation disrupted morphology and protein expression within the dentoalveolar complex. Ectopic matrix formation in pulp chambers, odontoblast layer disruption, narrowing of periodontal ligament space, and alteration of cementum structure were observed in histological and electron microscopy sections. Because serum P(i) levels are dramatically elevated in Fgf23(-/-), we assayed for apoptosis and expression of members from the small integrin-binding ligand, N-linked glycoprotein (SIBLING) family, both of which are sensitive to elevated P(i) in vitro. Unlike X-linked hypophosphatemic (Hyp) and wild-type (WT) specimens, numerous apoptotic osteocytes and osteoblasts were detected in Fgf23(-/-) specimens. Further, in comparison to Hyp and WT samples, decreased bone sialoprotein and elevated dentin matrix protein-1 protein levels were observed in cementum of Fgf23(-/-) mice. Additional dentin-associated proteins, such as dentin sialoprotein and dentin phosphoprotein, exhibited altered localization in both Fgf23(-/-) and Hyp samples. Based on these results, we propose that FGF23 and (P(i)) homeostasis play a significant role in maintenance of the dentoalveolar complex.
Anat Rec (Hoboken) 2010 Jul
PMID:Ablation of systemic phosphate-regulating gene fibroblast growth factor 23 (Fgf23) compromises the dentoalveolar complex. 2058 65

Biliary atresia (BA) is a rare neonatal disease characterized by inflammation and obstruction of the extrahepatic bile ducts (EHBDs). The Sox17-haploinsufficient (Sox17+/- ) mouse is an animal model of BA that encompasses bile duct injury and subsequent BA-like inflammation by the neonatal stage. Most Sox17+/- neonates die soon after birth, but some Sox17+/- pups reach adulthood and have a normal life span, unlike human BA. However, the phenotype and BA-derived scars in the hepatobiliary organs of surviving Sox17+/- mice are unknown. Here, we examined the phenotypes of the hepatobiliary organs in post-weaning and young adult Sox17+/- mice. The results confirmed the significant reduction in liver weight, together with peripheral calcinosis and aberrant vasculature in the hepatic lobule, in surviving Sox17+/- mice as compared with their wild-type (WT) littermates. Such hepatic phenotypes may be sequelae of hepatobiliary damage at the fetal and neonatal stages, a notion supported by the slight, but significant, increases in the levels of serum markers of liver damage in adult Sox17+/- mice. The surviving Sox17+/- mice had a shorter gallbladder in which ectopic hepatic ducts were more frequent compared to WT mice. Also, the surviving Sox17+/- mice showed neither obstruction of the EHBDs nor atrophy or inflammation of hepatocytes or the intrahepatic ducts. These data suggest that some Sox17+/- pups with BA naturally escape lethality and recover from fetal hepatobiliary damages during the perinatal period, highlighting the usefulness of the in vivo model in understanding the hepatobiliary healing processes after surgical restoration of bile flow in human BA.
Anat Rec (Hoboken) 2020 12
PMID:Anatomical and histological characteristics of the hepatobiliary system in adult Sox17 heterozygote mice. 3247 76