5 resultados para Respiratory function tests
em Chinese Academy of Sciences Institutional Repositories Grid Portal
Resumo:
An introduction to a modified forced oscillation method, square-wave excitation technique, including fundamentals and methods, as used in respiratory function examination. On the basis of experimental results and theoretical predictions, we suggest that Respiratory Acoustic Impedance (RAI) measurement by spectral analysis can significantly improve estimation of contribution to RAI from different part of respiratory tract. The outcome is of considerable interest in the study of lung disease, such as COPD and asthma in young children.
Resumo:
The reaction between an indium over layer and high purity MBE grown n-ZnSe chlorine doped (2x 10(18) cm-3) epilayers has been investigated using X-ray diffraction, Rutherford backscattering spectroscopy, X-ray photoelectron and Auger electron spectroscopy, and by electrical function tests (I-V and C-V). Good ohmic contacts were formed after annealing at 250 or 300-degrees-C for a few minutes in forming gas. Annealing at lower or higher temperatures resulted in higher resistance or rectifying contacts. The data show that no compounds were formed at the interface; instead In appeared to diffuse into the ZnSe. High surface doping densities appear to allow an ohmic contact, but the electrical data suggest that compensation effects are also very significant in the formation of the contact. These effects must be considered for successful formation of the ohmic contact.
Resumo:
Three homologous short-chain neurotoxins, named NT1, NT2 and NT3, were purified from the venom of Naja kaouthia. NT1 has an identical amino acid sequence to cobrotoxin from Naja naja atra [Biochemistry 32 (1993) 2131]. NT3 shares the same sequence with cobrotoxin b [J. Biochem. (Tokyo) 122 (1997) 1252], whereas NT2 is a novel 6 1 -residue neurotoxin. Tests of their physiological functions indicate that NT1 shows a greater inhibition of muscle contraction induced by electrical stimulation of the nerve than do NT2 and NT3. Homonuclear proton two-dimensional NMR methods were utilized to study the solution tertiary structure of NT2. A homology model-building method was employed to predict the structure of NT3. Comparison of the structures of these three toxins shows that the surface conformation of NT1 facilitates the substituted base residues, Arg28, Arg30, and Arg36, to occupy the favorable spatial location in the central region of loop 11, and the cation groups of all three arginines face out of the molecular surface of NT1 This may contribute greatly to the higher binding of NT1 with AchR compared to NT2 and NT3. (C) 2002 Elsevier Science B,V. All rights reserved.
Resumo:
Deaths from microcystin toxication have widely been attributed to hypovolemic shock due to hepatic interstitial hemorrhage, while some recent studies suggest that cardiogenic complication is also involved. So far, information on cardiotoxic effects of MC has been rare and the underlying mechanism is still puzzling. The present study examined toxic effects of microcystins on heart muscle of rats intravenously injected with extracted MC at two doses, 0.16LD(50) (14 mu g MC-LReq kg(-1) body weight) and 1LD(50) (87 mu g MC-LReq kg(-1) body weight). In the dead rats, both TTC staining and maximum elevations of troponin I levels confirmed myocardial infarction after MC exposure, besides a serious interstitial hemorrhage in liver. In the 1LD(50) dose group, the coincident falls in heart rate and blood pressure were related to mitochondria dysfunction in heart, while increases in creatine kinase and troponin I levels indicated cardiac cell injury. The corresponding pathological alterations were mainly characterized as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. MC administration at a dose of 1LD(50) not only enhanced activities and up-regulated mRNA transcription levels of antioxidant enzymes, but also increased GSH content. At both doses, level of lipid peroxides increased obviously, suggesting serious oxidative stress in mitochondria. Simultaneously. complex I and III were significantly inhibited, indicating blocks in electron flow along the mitochondrial respiratory chain in heart. In conclusion, the findings of this study implicate a role for MC-induced cardiotoxicity as a potential factor that should be considered when evaluating the mechanisms of death associated with microcystin intoxication in Brazil. (C) 2009 Elsevier Ireland Ltd. All rights reserved.