Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the time course of disulfide bond formation by iodine oxidation (in a methanolic and hydrochloric acid solution) of a cysteinyl(S-acetamidomethyl)-glutaminyl tridecapeptide, we observed by ESI, FAB mass spectrometry (pseudo-molecular ion and ion-fragments) and 1H-NMR a side reaction due to a shift of the Acm leaving group from cysteine to the carboxamide side chain of glutamine. This type of Acm-shift at low level was described previously by L.W. Mendelson et al. (Int. J. Pept. Protein Res. 35:249-257) for an aspariginyl-cysteinyl(S-acetamidomethyl) peptide in an anhydrous hydrochloric solution. We report here the efficiency of glutamine as a scavenger to suppress the S-->N shift of the acetamidomethyl group during S-acetamidomethyl cleavage and sulfhydryl oxidation with iodine, as the folded tridecapeptide was obtained with the expected molecular weight.
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PMID:Side reaction of S-to-N acetamidomethyl shift during disulfide bond formation by iodine oxidation of S-acetamidomethyl-cysteine in a glutamine-containing peptide. 883 14

Almost all respiratory diseases except benign lung tumors and lung dysplasia entail acute lung injury. The many clinical conditions associated with acute lung injury include aspiration pneumonia, bacterial pneumonia, and sepsis. The fundamental cause of acute lung injury is pulmonary vascular hyperpermeability. Pulmonary vascular hyperpermeability can be attenuated by nitric oxide and cyclic GMP, and potentiated by oxygen radicals and elastase released from neutrophils. Adhesion molecule inhibition could become an effective therapy against acute lung injury, because the adhesion molecules are very important in the pathogenesis of this condition. Adhesion molecules could also be useful markers of disease activity in various lung diseases. Neutrophil elastase inhibitors may become important as therapeutic agents against acute exacerbations of idiopathic interstitial pneumonia, because this pathological condition is a type of acute lung injury. Similarly, N-acetyl cysteine could also become a useful therapeutic agent against idiopathic interstitial pneumonia, because it is a precursor of glutathione, which is the major antioxidant in the fluid lining of the bronchial epithelium.
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PMID:[Pathophysiology of acute lung injury]. 921 75

Neurodegeneration with brain iron accumulation (NBIA), or Hallervorden- Spatz disease, is an extremely rare autosomal recessive disorder with cysteine-iron complex accumulation in globus pallidus, seen histopathologically. Magnetic resonance imaging offers an opportunity for diagnosis; however, therapeutic options are still ineffective. We report a case of 13-year-old girl, symptomatic since the age of three years with dystonia, poor scholastic performance and speech disturbances. She was admitted with aspiration pneumonia, and died before she could be investigated. Examination of brain at autopsy revealed iron deposition in bilateral globus pallidi, confirmed by special stains and elemental dispersion analysis by spectrometry and a diagnosis of Hallervorden- Spatz disease or NBIA was made. This report highlights the importance of autopsy and scanning electron microscopic examination in unsuspected cases where cause of death is not known.
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PMID:Autopsy always teach and tell: neurodegeneration with brain iron accumulation: a case report. 1830 57

We have used pulsed electron-electron double resonance (PELDOR) spectroscopy to measure the distance between spin labels at Cys(133) of the regulatory region of TnI (TnI133) and a native or genetically substituted cysteine of TnC (TnC44, TnC61, or TnC98). In the +Ca(2+) state, the TnC44-TnI133-T distance was 42 A, with a narrow distribution (half-width of 9 A), suggesting that the regulatory region binds the N-lobe of TnC. Distances for TnC61-TnI133 and TnC98-TnI133 were also determined to be 38 A (width of 12 A) and 22 A (width of 3.4 A), respectively. These values were all consistent with recently published crystal structure (Vinogradova, M. V., Stone, D. B., Malanina, G. G., Karatzaferi, C., Cooke, R., Mendelson, R. A., and Fletterick, R. J. (2005) Proc. Natl Acad. Sci. U.S.A. 102, 5038-5043). Similar distances were obtained with the same spin pairs on a reconstituted thin filament in the +Ca(2+) state. In the -Ca(2+) state, the distances displayed broad distributions, suggesting that the regulatory region of TnI was physically released from the N-lobe of TnC and consequently fluctuated over a variety of distances on a large scale (20-80 A). The interspin distance appeared longer on the filament than on troponin alone, consistent with the ability of the region to bind actin. These results support a concept that the regulatory region of TnI, as a molecular switch, binds to the exposed hydrophobic patch of TnC and traps the inhibitory region of TnI away from actin in Ca(2+) activation of muscle.
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PMID:Switch action of troponin on muscle thin filament as revealed by spin labeling and pulsed EPR. 2013 80