Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have analyzed the effect of extracellular stimuli on the differentiation state of the CA77 thyroid C-cell line as a model to understand the control of neural crest cell differentiation. In contrast to the endocrine C-cell phenotype, we found that CA77 cells have a neuronal phenotype characterized by laminin-induced neurites, neuronal antigens, and calcitonin gene-related peptide (CGRP) mRNA expression. Treatment with dexamethasone and retinoic acid reversibly repressed some of these neuronal characteristics to induce features more characteristic of the parental C-cells. In the case of dexamethasone treatment, there was a partial retraction and thinning of neurites, an increased number of secretory vesicles in the cell bodies, and about a 10-fold decrease in DNA synthesis. Treatment with retinoic acid alone or in combination with dexamethasone caused decreased cell adhesion and an even more extensive retraction of the neurites. Dexamethasone also biased the steady state levels of the alternatively spliced transcripts from the calcitonin/CGRP gene to favor calcitonin relative to CGRP mRNA. While retinoic acid treatment decreased both calcitonin and CGRP mRNA levels, the combination of dexamethasone and retinoic acid still yielded the increase in calcitonin relative to CGRP mRNA. These results suggest that glucocorticoids and retinoic acid may contribute to a late and reversible differentiation of thyroid C-cells by partly repressing neuronal properties.
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PMID:Neuronal properties of a thyroid C-cell line: partial repression by dexamethasone and retinoic acid. 156 64

The growth and differentiation of epidermal cells in vitro show a marked dependence on the calcium concentration of the medium. In this study the effect of experimentally produced hyper- and hypocalcaemia on the rat epidermis in vivo has been investigated. Hypercalcaemia, induced by injections of calcium chloride, produced a decrease in epidermal labelling index and some epidermal thinning. On the other hand hypocalcaemia, induced by calcitonin, failed to lead to changes in these measurements. The diurnal variation in epidermal labelling index and serum calcium levels was also measured. Whilst the labelling index decreased considerably over the period 09.00 hours to 18.00 hours, no significant changes were observed in serum calcium. These results suggest that while, under certain circumstances in vivo, the epidermal cell shows the same sensitivity to calcium as it does in vitro, calcium is not a major regulator of epidermopoiesis.
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PMID:The effect of serum calcium levels on the rate of epidermal renewal in the rat. 654 May 96

Denervation in man often results in shiny, dry, thin skin. A previous study has shown that the epidermis of glabrous skin in the rat becomes approximately 40% thinner within 1 week following sciatic nerve transection, but which nerve fiber type or types influence epidermal thickness is unknown. In this study, we compared the effects on the epidermis of selective sensory, motor, and sympathetic denervation. Protein gene product 9.5 and calcitonin gene-related peptide immunocytochemical staining were used to determine the extent of denervation of epidermis, dermis, and sweat glands in the footpads. Epidermal thickness of the glabrous plantar skin of the foot was measured. To verify the specificity and reliability of each animal model, the relevant regions of the peripheral nervous system were examined by light or electron microscopy or both. Epidermal thickness decreased significantly following sciatic nerve transection (58% of control, P < 0.05) and dorsal root ganglionectomy (59%; P < 0.05). The thickness also decreased following lumbar ventral rhizotomy (61%; P < 0.01), destruction of lumbar spinal motor neurons (66%; P < 0.05), and botulinum toxin-induced paralysis of the tibialis anterior and gastrocnemius muscles (70%; P < 0.05). A slight decrease followed dorsal rhizotomy (84%; P < 0.01). In contrast, no significant alterations in epidermal thickness were detected following sham operation and sympathectomy. Epidermal thinning was paralleled by reductions in the amounts of transcripts for glyceraldehyde-3-phosphate dehydrogenase and beta-actin. These results suggest that selective loss of both sensory and motor fibers to the hind limb can contribute to reducing epidermal thickness in rat foot glabrous skin.
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PMID:Sensory and motor denervation influence epidermal thickness in rat foot glabrous skin. 934 69

Glucocorticoids are important drugs in the treatment of variety diseases, but long-term period use can lead to various adverse effects, including osteoporosis. Glucocorticoid-induced osteoporosis is mainly caused by inhibition of osteoblastic bone formation, which results not only in decreased bone mineral density, but reduction of bone strength by trabecular thinning in bone microstructures. The evidence suggests that daily oral glucocorticoid doses higher than 5 mg prednisolone or equivalent increase the risk of fracture within 3-6 months after the start of therapy. High-dose inhaled glucocorticoids may also increase fracture risk. The diagnostic procedures are similar to those for primary osteoporosis, but the diagnostic threshold for bone mineral density needs to be higher than that for primary osteoporosis. Treatment with vitamin D, calcitonin, sex hormone replacement, and bisphosphonates has been shown to be effective, and bisphosphonates have been demonstrated to be the most valuable drugs for glucocorticoid-induced osteoporosis. There are several lines of evidence indicating that they are effective in preventing and treating low bone mineral density and in reducing fracture risk.
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PMID:Glucocorticoid-induced osteoporosis. 1551 6

The maternal skeleton rapidly demineralizes during lactation to provide calcium to milk, responding to the stimuli of estrogen deficiency and mammary-secreted PTH-related protein. We used calcitonin/calcitonin gene-related peptide-alpha (Ctcgrp) null mice to determine whether calcitonin also modulates lactational mineral metabolism. During 21 d of lactation, spine bone mineral content dropped 53.6% in Ctcgrp nulls vs. 23.6% in wild-type (WT) siblings (P < 0.0002). After weaning, bone mineral content returned fully to baseline in 18.1 d in Ctcgrp null vs. 13.1 d in WT (P < 0.01) mice. Daily treatment with salmon calcitonin from the onset of lactation normalized the losses in Ctcgrp null mice, whereas calcitonin gene-related peptide-alpha or vehicle was without effect. Compared with WT, Ctcgrp null mice had increased circulating levels of PTH and up-regulation of mammary gland PTH-related protein mRNA. In addition, lactation caused the Ctcgrp null skeleton to undergo more trabecular thinning and increased trabecular separation compared with WT. Our studies confirm that an important physiological role of calcitonin is to protect the maternal skeleton against excessive resorption and attendant fragility during lactation and reveal that the postweaning skeleton has the remarkable ability to rapidly recover even from losses of over 50% of skeletal mineral content.
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PMID:Calcitonin plays a critical role in regulating skeletal mineral metabolism during lactation. 1691 34

An 82-year-old diabetic female had been aware of gradually enlarging, painless scalp depressions in the bilateral parietal regions for more than 6 years. She had no history of head injury, or inflammatory or malignant disease. Her family history was unremarkable for hereditary bone disease. She had diabetes mellitus which had been well controlled with orally administered drugs. Blood examination showed normal renal and liver functions with normal serum calcium, magnesium, and phosphorus concentrations, in addition to normal parathyroid hormone and calcitonin levels. Neuroimaging including skull radiography, head computed tomography, and magnetic resonance imaging demonstrated symmetric thinning in the bilateral parietal bones attributed to loss of diploe and thinning of the outer table. The inner table was intact without associated soft tissue mass or vascular lesions. Technetium-99m methylene diphosphate systemic bone scintigraphy showed mild hypoaccumulation in the affected calvarium on the left. No other pathological findings were found by systemic examination. She underwent open biopsy for histological verification which revealed homogeneous membranous bone tissue with regressed diploe, absence of osteoblasts, absence of osteoclastic appearance, and absence of findings of underlying malignancy. There was no markedly fibrovascular connective tissue typical of Gorham-Stout disease. Calvarial thinning in the present case may have been caused by an undetermined complex mechanism.
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PMID:Idiopathic calvarial thinning. 1857 36

Innervation is required to preserve several aspects of skin homeostasis. Previous studies in rodents have shown that sciatic nerve transection leads to epidermal thinning and reduced keratinocyte proliferation. As the sciatic nerve is composed of sensory and motor axons, it is not clear whether skin alterations reflect motor or sensory disturbances. In this study, we used neonatal capsaicin treatment to evaluate whether sensory chemical denervation affects keratinocyte proliferation at 1, 3, and 6 months of age. Using design-based stereological methods, we estimated the total length of intraepidermal nerve fibers (IENF) that were of peptidergic type and the number of bromodeoxyuridine-labeled (BrdU(+) ) nuclei in the hind paw glabrous epidermis of control and capsaicin-treated rats. We found that the treatment decreased the total fiber length of IENF immunoreactive for both protein gene product 9.5 (PGP(+) ) and of IENF immunoreactive for calcitonin gene-related peptide (CGRP(+) ). The length of PGP(+) fibers decreased by 83%, 81%, and 77% and that of CGRP(+) fibers decreased by 48%, 58%, and 58% at 1, 3, and 6 months, respectively. Double-immunofluorescence staining for neural beta III tubulin and CGRP revealed that the majority of the remaining fibers in the epidermis after capsaicin treatment were of peptidergic type. The number of BrdU(+) nuclei was similar in both groups. Our findings suggest that IENF present after capsaicin treatment are sufficient to maintain epidermal replacement.
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PMID:Long-term effects of neonatal capsaicin treatment on intraepidermal nerve fibers and keratinocyte proliferation in rat glabrous skin. 2115 28

Osteoporosis is a common bone metabolic disease in caged laying hens. This disease affects animal welfare and economic costs. In this study, a model of osteoporosis induced by low dietary phosphorus was established. A total of sixty 22-week-old Roman white laying hens were randomly divided into two groups, including a control group (group C) and a low dietary phosphorus group (group P). The effects of low dietary phosphorus on the endocrine and tibial osteoprotegerin (OPG)/nuclear factor kappa B receptor activating factor ligand (RANKL) signaling pathways of osteoporosis in caged laying hens were analyzed by serology, bone biomechanics, molecular biology and histopathology. The results showed that low dietary phosphorus decreased the production performance, and egg quality of laying hens and increased the contents of serum calcium (Ca), osteocalcin (OCN), alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRACP). The contents of serum phosphorus, calcitonin (CT), OPG and tibial biomechanics index decreased. The bone mineral density (BMD), cortical bone thickness and the expression level of OPG protein in tibia decreased. The expression of OCN, nuclear factor kappa B receptor activating factor (RANK) and RANKL protein increased. Low dietary phosphorus caused thinning and fracture of the bone trabeculae and enlargement of the bone marrow cavity of tibia. Our results suggest that phosphorus may affect bone metabolism by regulating the OPG/RANKL signaling pathway.
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PMID:Effects of low dietary phosphorus on tibia quality and metabolism in caged laying hens. 3252 47