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 gas exchange region of newborn rats is composed of large thick-walled gas exchange saccules that become subdivided by septum formation between ages 4 and 14 days. Dexamethasone given daily from age 4 to 13 days irreversibly prevents septation. We now asked if dexamethasone (0.1 micrograms) given daily from age 4 to 13 days accelerates alveolar wall thinning and alters wall composition. Compared with controls, within 2 days dexamethasone-treated pups had a 20% thinner gas exchange wall, a 35% lower volume density (Vv) and absolute volume of interstitial fibroblasts, and a 45% greater Vv of type II cells. At age 14 days the volumes of type I cells, fibroblasts, and acellular matrix were approximately 35% less in dexamethasone-treated pups, but the volumes of type II and endothelial cells did not exhibit significant intergroup differences. We conclude dexamethasone accelerates alveolar wall thinning and suggest dexamethasone diminishes replication of fibroblasts more rapidly than it diminishes division of type II, impairs conversion of type II to I, and does not decrease replication of endothelial cells.
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PMID:Dexamethasone accelerates postnatal alveolar wall thinning and alters wall composition. 374 Mar 2

A subjective retrospective analysis of 250 patients was done to better understand a serious long-term complication of inflatable implants. A series of 397 breasts with inflatable prostheses exhibited 32% thinning of the breast tissue. Fifty-six percent of the thinning was found in the first 2 years, and 74% by 3 years. Of those breasts that thinned, 31.5% exhibited the streaking phenomenon. Breasts were divided into categories of bilateral Decadron addition, right-sided addition, and no addition. All groups showed roughly 30% thinning with equal right-sided and left-sided distribution. No treatment is needed for mild thinning (41% of this series), but a change to a gel prosthesis is advocated for more severe cases. Breast thinning following inflatable implants is thought to be related to pressure atrophy, not to the addition of steroids. Generalized tissue malacia has not been seen with the use of gel prostheses. With longer follow-up a higher rate of thinning is anticipated. From this study it is believed the inflatable implant is not the prosthesis of choice, and its use has been discontinued by the author.
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PMID:Breast thinning and streaking following the use of inflatable implants--a subjective clinical study. 746 23

Postnatal formation of alveoli can be largely prevented by glucocorticoid treatment, which accelerates alveolar wall thinning and inhibits outgrowth of new interalveolar septa. Since a double capillary network is a prerequisite for interalveolar wall formation, we hypothesized that glucocorticoid treatment inhibited alveolar formation, indirectly, by inducing precocious microvascular maturation. Between 4 and 60 days we followed up qualitatively and quantitatively the effects of 2 weeks (days 2-15) of daily Decadron (Dexamethasone phosphate) injections on the lung structure. Glucocorticoid induced only small changes in body weight or lung volume. However, during the first 2 weeks, it accelerated alveolar wall thinning and microvascular maturation and partly suppressed the outgrowth of new interalveolar septa. In Decadron-treated rats, the interstitial tissue mass was significantly reduced during the first 2 weeks, and a larger alveolar surface area was endowed with a capillary monolayer on days 10 and 13. One week after drug withdrawal, the trend towards precocious maturation of the lung was reversed. Lipofibroblasts reappeared, and inter-airspace septa regressed towards a more immature state. We found indications of a second burst of alveolization by resumption of secondary septa formation. The late sequelae of Decadron treatment (day 60) were manifested as an 'emphysematous' condition of the lungs, with larger and fewer airspaces, the delayed alveolization being insufficient to compensate for the initial deficit.
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PMID:Influence of postnatally administered glucocorticoids on rat lung growth. 858 Feb 14

While prefrontal lesions in rodents serve as models for frontal lobe syndromes, neonatal lesions are considered as models for disconnection syndromes, such as schizophrenia. We investigated the effect of neonatal lesions of the rat medial prefrontal cortex (mPFC) together with pubertal dexamethasone-challenge on adult rat behaviour and on apomorphine-induced behavioural changes. Adult lesions were used as controls. Rats with neonatal (postnatal day 7) or adult excitotoxic lesions or sham-lesions of the mPFC were tested 9 weeks after surgery. At postnatal day 49 one group of neonatal operated rats were systemically injected with the glucocorticoid receptor agonist dexamethasone (20 mg/kg), in order to simulate stress-induced glucocorticoid receptor activation. Working memory and perseveration was tested in T-maze tasks (continuous delayed alternation and reversal learning). Additionally, locomotor activity and prepulse inhibition (PPI) of startle was tested with and without apomorphine-treatment. Brain tissue damage was assessed using Nissl-staining and parvalbumine-immunocytochemistry. Pronounced thinning of the prelimbic-infralimbic subregion of the mPFC accompanied by altered cytoarchitecture and reduced number of parvalbumine-immunopositive neurones was found after neonatal lesions while adult lesions resulted in loss of neurones accompanied by gliosis. Neonatal lesions increased perseveration in the T-maze tasks and enhanced PPI, while adult lesions induced a working memory deficit. This differential behavioural outcome presumably reflects neurodevelopmentally induced alterations in neuronal circuits after neonatal lesions versus damage to mPFC alone after adult lesions. Dexamethasone-injection at day 49 did not alter behaviour in these tasks. Motor activity was not affected by neonatal or adult lesions but dexamethasone reduced apomorphine-induced hyperlocomotion.
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PMID:Effects of neonatal lesions of the medial prefrontal cortex on adult rat behaviour. 1521 3

Could it be the thinning of the ozone layer (see p. 645) that has indirectly caused our baffling faux pas in recent issues? In reporting the formation by the National Academy of Sciences of a Committee on Environmental Research to be headed by Cornell President Emeritus Dale Corson (11 October, p. 192), we inexplicably fused the distinguished careers of physicist Corson and former Dartmouth president John Kemeny. It was the latter who headed the President's Commission that investigated the accident at Three Mile Island, whereas Corson's distinctions include heading the NAS's "Corson Panel" on scientific communications and national security and founding the Government-University-Industry Research Roundtable. Three weeks earlier (in "Mycomummy," 20 September, p. 1353), we misspelled Coccidioides, a fungus whose petrified spores were found in the ancient skeleton of a Sinaguan indian.
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PMID:Errata. 1777 83

Glaucoma is a leading cause of irreversible blindness worldwide. Current treatments of glaucoma involve lowering the IOP by means of decreasing aqueous humor production or increasing non-trabecular aqueous humor outflow with the help of IOP-lowering eye drops, nanotechnology enabled glaucoma drainage implants, and trabeculectomy. However, there is currently no effective and permanent cure for this disease. In order to investigate new therapeutic strategies, three dimensional (3D) biomimetic trabecular meshwork (TM) models are in demand. Therefore, we adapted MAX8B, a peptide hydrogel system to bioengineer a 3D trabecular meshwork scaffold. We assessed mechanical and bio-instructive properties of this engineered tissue matrix by using rheological analysis, 3D cell culture and imaging techniques. The scaffold material exhibited shear-thinning ability and biocompatibility for proper hTM growth and proliferation indicating a potential utilization as an injectable implant. Additionally, by using a perfusion system, MAX8B scaffold was tested as an in vitro platform for investigating the effect of Dexamethasone (Dex) on trabecular meshwork outflow facility. The physiological response of hTM cells within the scaffold to Dex treatment clearly supported the effectiveness of this 3D model as a drug-testing platform, which can accelerate discovery of new therapeutic targets for glaucoma. STATEMENT OF SIGNIFICANCE: Artificial 3D-TM (3-dimentional Trabecular Meshwork) developed here with hTM (human TM) cells seeded on peptide-hydrogel scaffolds exhibits the mechanical strength and physiological properties mimicking the native TM tissue. Besides serving a novel and effective 3D-TM model, the MAX8B hydrogel could potentially function as an injectable trabecular meshwork implant.
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PMID:An injectable peptide hydrogel for reconstruction of the human trabecular meshwork. 3155 33