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)

Reconstruction of the nasal ala demands a two-layer reconstruction with or without a cartilaginous support. Many techniques are described: most of them need several stages either by a delayed procedure or by secondary thinning. Often the external skin is taken from the surrounding area, but the texture of the skin is different and obvious scars may result. Therefore, we suggest using a rotation flap from the glabella combined with a trap-door flap from the nose or the septum. A thin, well-shaped nasal ala can thus be rebuilt without additional obvious scars.
HNO 1990 Jan
PMID:[Reconstruction of the nasal ala with a glabella flap]. 217 75

This study was performed to examine the roles of body temperature, NMDA receptors and nitric oxide (NO) synthase in post-ischemic retinal injury in rats. Cell loss in the ganglion cell layer and thinning of the inner plexiform layer were observed 7 days after ischemia. Cell loss in the ganglion cell layer but not thinning of the inner plexiform layer was reduced by hypothermia during ischemia. Intravenous injection of dizocilpine (MK-801) or Nomega-nitro-L-arginine methyl ester (L-NAME) prior to ischemia ameliorated retinal injury. These results suggest that activation of NO synthase following NMDA receptor stimulation is involved in ischemia-induced retinal injury.
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PMID:Inhibition of NMDA receptors and nitric oxide synthase reduces ischemic injury of the retina. 968 14

Nitric oxide (NO) is a pleiotropic signaling molecule that is produced by bone cells constitutively and in response to diverse stimuli such as proinflammatory cytokines, mechanical strain, and sex hormones. Endothelial nitric oxide synthase (eNOS) is the predominant NOS isoform expressed in bone, but its physiological role in regulating bone metabolism remains unclear. Here we studied various aspects of bone metabolism in female mice with targeted disruption of the eNOS gene. Mice with eNOS deficiency (eNOS KO) had reduced bone mineral density, and cortical thinning when compared with WT controls and histomorphometric analysis of bone revealed profound abnormalities of bone formation, with reduced osteoblast numbers, surfaces and mineral apposition rate. Studies in vitro showed that osteoblasts derived from eNOS KO mice had reduced rates of growth when compared with WT and were less well differentiated as reflected by lower levels of alkaline phosphatase activity. Mice with eNOS deficiency lost bone normally following ovariectomy but exhibited a significantly blunted anabolic response to high dose exogenous estrogen. We conclude that the eNOS pathway plays an essential role in regulating bone mass and bone turnover by modulating osteoblast function.
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PMID:Defective bone formation and anabolic response to exogenous estrogen in mice with targeted disruption of endothelial nitric oxide synthase. 1115 48

We compared the degree of neurotoxic outcome in the retina exposed to three nitric oxide (NO) donors with different half-life of NO release. Intravitreal injection of NO donors resulted in a significant decrease in cell density in the ganglion cell layer and thinning of the inner plexiform layer in a half-life time-dependent manner. Concurrent injection of an NO-trapping reagent with an NO donor abolished NO donor-induced retinal damage. (+)-MK-801 also prevented NO-induced retinal damage, indicating that N-methyl-D-aspartate receptors are partly involved in NO-induced neurodegeneration. These results may be relevant to a pathogenic role of NO - glutamate receptor in several ophthalmic disorders.
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PMID:Retinal neurotoxicity of nitric oxide donors with different half-life of nitric oxide release: involvement of N-methyl-D-aspartate receptor. 1293 29

Progressive thinning of the scalp hair in androgenetic alopecia (AGA) results in a gradual decline in natural protection of the scalp from ultraviolet radiation (UVR). A number of pathologic conditions of the scalp are evidently related to UVR, particularly photosensitive diseases and disorders of the chronically photodamaged bald scalp. The most important chronic effects of UVR are photocarcinogenesis and solar elastosis. Besides these, erosive pustular dermatosis and 'red scalp' are distinct disorders peculiar to the balding scalp. While the consequences of sustained UVR on the unprotected scalp are well appreciated, the effects of UVR on hair loss have widely been ignored. However, clinical observations and theoretical considerations suggest that UVR may have negative effects: acute telogen effluvium from UVR has been described, and the production of porphyrins by Propionibacterium sp. in the pilosebaceous duct, with photoactivation of porphyrins leading to oxidative tissue injury, has been implicated in follicular microinflammation. Alternatively, keratinocytes themselves may respond to physicochemical stress from UVR, besides irritants and pollutants, by producing radical oxygen species and nitric oxide and by releasing proinflammatory cytokines, eventually leading to injury of the putative site of follicular stem cells in the superficial portion of the hair follicle. Since all of these processes involved in hair loss share the common feature that they are induced or exacerbated by exposure to sunlight, it is proposed that AGA is a photoaggravated dermatosis that requires photoprotection.
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PMID:Is androgenetic alopecia a photoaggravated dermatosis? 1465 23

Two common non-steroidal anti-inflammatory drugs (NSAIDs) and their nitric oxide (NO) adducts were evaluated for effects on stomach and thymus. Following 4-h duration (acute) oral dosing of fasted male Wistar rats, 1.33 x 10(-4)mol/kg of ibuprofen caused significant visual irritation score and microscopic thinning, although an ulceration assay proved insensitive. Ibuprofen esterified with NO abolished irritation and significantly reduced thinning. Gastro-protective effects of NO-linked ibuprofen were associated with higher levels of diaphorase by optical density, an enzymatic marker of local synthesis of nitric oxide. Both indomethacin and its congener at 2 x 10(-5)mol/kg produced microscopic signs of thinning only, not visible irritation or alteration of diaphorase staining. Results suggest that NO-linked ibuprofen can promote resistance to mucosal injury, possibly via local synthesis of NO. All NO-congeners and parent NSAIDs produced comparable reductions in the abundance of medullary nitrergic cells, those synthesising NO in thymus, without significantly lowering T-cellularity, the relative size of cortex wherein T-cells are produced. Findings indicate disturbance of T-cell tolerance, consistent with increased risk of autoimmune susceptibility.
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PMID:Gastric and thymic assay of acute oral treatment of rats with nitric oxide esters of ibuprofen or indomethacin. 1601 70

Keratoconus, a non-inflammatory thinning of the cornea, is a leading indication for corneal transplantation. For its causation, we propose a "Cascade Hypothesis" stating that keratoconus corneas have abnormal or defective enzymes in the lipid peroxidation and/or nitric oxide pathways leading to oxidative damage. The accumulation of oxidative, cytotoxic by-products causes an alteration of various corneal proteins, triggering a cascade of events, (i.e. apoptosis, altered signaling pathways, increased enzyme activities, fibrosis). This hypothesis is supported by biochemical, immunohistochemical and molecular data presented in this review. Based upon this evidence, one can speculate that keratoconus patients should minimize their exposure to oxidative stress. Protective steps should include wearing ultraviolet (UV) protection (in the contact lenses and/or sunglasses), minimizing the mechanical trauma (eye rubbing, poorly fit contact lenses) and keeping eyes comfortable with artificial tears, non-steroidal anti-inflammatory drugs and/or allergy medications.
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PMID:The cascade hypothesis of keratoconus. 1630 9

Using simultaneous nitric oxide and carbon monoxide lung transfer measurements (T(LNO) and T(LCO)), the membrane transfer capacity (D(m)) and capillary lung volume (V(c)) as well as the dimensionless ratio T(LNO)/T(LCO) can be calculated. The significance of this ratio is yet unclear. Theoretically, the T(LNO)/T(LCO) ratio should be inversely related to the product of both lung alveolar capillary membrane (mu) and blood sheet thicknesses (K). NO and CO transfers were measured in healthy subjects in various conditions likely to be associated with changes in K and/or mu. Experimentally, deflation of the lung from 7.4 to 4.8 l decreased the T(LNO)/T(LCO) ratio from 4.9 to 4.2 (n=25) which was consistent mainly with a thickening of the blood sheet. Compared with continuous negative pressure breathing, continuous positive pressure breathing increased this ratio suggesting a thinning of the capillary sheet. It was also observed with 12 healthy subjects that slight haemodilution that may thicken the blood sheet decreased the T(LNO)/T(LCO) ratio from 4.85 to 4.52. In conclusion, the T(LNO)/T(LCO) ratio is related to the thickness of the alveolar blood barrier. This ratio provides novel information for the analysis of the diffusion properties.
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PMID:Deciphering the nitric oxide to carbon monoxide lung transfer ratio: physiological implications. 1749 39

We assessed the role of nitric oxide (NO) and the kinin B2 receptor in mediating tissue kallikrein's actions in intramyocardial inflammation and cardiac remodeling after ischemia/reperfusion (I/R) injury. Adenovirus carrying the human tissue kallikrein gene was delivered locally into rat hearts 4 days prior to 30-minute ischemia followed by 24-hour or 7-day reperfusion with or without administration of icatibant, a kinin B2 receptor antagonist, or N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor. Kallikrein gene delivery improved cardiac contractility and diastolic function, reduced infarct size at 1 day after I/R without affecting mean arterial pressure. Kallikrein treatment reduced macrophage/monocyte and neutrophil accumulation in the infarcted myocardium in association with reduced intercellular adhesion molecule-1 levels. Kallikrein increased cardiac endothelial nitric oxide synthase phosphorylation and NO levels and decreased superoxide formation, TGF-beta1 levels and Smad2 phosphorylation. Furthermore, kallikrein reduced I/R-induced JNK, p38MAPK, IkappaB-alpha phosphorylation and nuclear NF-kappaB activation. In addition, kallikrein improved cardiac performance, reduced infarct size and prevented ventricular wall thinning at 7 days after I/R. The effects of kallikrein on cardiac function, inflammation and signaling mediators were all blocked by icatibant and L-NAME. These results indicate that tissue kallikrein through kinin B2 receptor and NO formation improves cardiac function, prevents inflammation and limits left ventricular remodeling after myocardial I/R by suppression of oxidative stress, TGF-beta1/Smad2 and JNK/p38MAPK signaling pathways and NF-kappaB activation.
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PMID:Nitric oxide mediates cardiac protection of tissue kallikrein by reducing inflammation and ventricular remodeling after myocardial ischemia/reperfusion. 1806 96

Spontaneous intestinal perforation (SIP) occurs commonly in extremely low birth weight (ELBW) infants. Our understanding of its etiologies has improved dramatically over the last decade. Included in this comprehension is an ongoing reconciliation of the iatrogenic risk factors, the microbiology, and the histopathology. The latter shows focal perforations with necrosis of the muscularis externa and no sign of ischemic damage (typically characterized by mucosal necrosis in the preterm bowel). Associations include extreme prematurity, early postnatal steroids (EPS), early use of indomethacin (EUI), and two common pathogens (Candida and Staphylococcus epidermis). Animal models of SIP suggest that all risk factors converge on a common collection of signaling pathways: those of nitric oxide synthases (NOS), insulin-like growth factors (IGFs), and epidermal growth factors (EGFs). Many of these factors skew trophism of the ileum (defined as thinning of the submucosa concomitant with hyperplasia of the muscosa). Global depletion of NOS is associated with disturbed intestinal motility and diminished transforming growth factor-alpha (TGF-alpha) in the muscularis externa. This constellation of insults seems to make the distal intestine vulnerable to perforation during recovery of motility.
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PMID:Understanding intestinal vulnerability to perforation in the extremely low birth weight infant. 1878 6


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