ビョウインマエ シンパイ テイシ ニオケル キュウキュウ キュウメイシ ノ キカン ソウカン ニツイテ : ホンケン ノ ゲンジョウ ト コンゴ ノ カダイ

Activities of Japanese Paramedics have increased and advanced year by year. Especially, intubation for OHCPA（out of hospital cardiopulmonary arrest） is approved since July 2004, but it is necessary to finish the training in Fire-fighter’s school and intubation practice in hospitals. In Fire-fighter’s school, Paramedics attend lectures and simulation, and in hospital, intubation practice for patients. Medical-control is the system for keeping the qualities and verification of details in the scene of pre-hospital medical care. This report discusses the states and problems of paramedic intubation, practice in hospital, airway management, from the questionnaire survey

Effect of aspirin treatment on serum levels of lipoprotein (a) : analysis from the apolipoprotein (a) isoforms

We have found that aspirin lowers elevated serum lipoprotein(a) [Lp(a)] levels via reduction of the transcriptional activity of apolipoprotein(a) [apo(a)] gene with suppression of apo(a) mRNA expression. In the present study, we evaluated the effect of aspirin treatment on serum Lp(a) level and analyzed its relation to type of apo(a) isoform. Serum levels of Lp(a) were measured by turbidimetric immunoassay before and after the oral administration of aspirin therapy (81 mg/day) in 57 patients with coronary artery disease or cerebral infarction. Apo(a) isoforms were determined by immunoblotting method. In patients with high serum Lp(a) levels (more than 30 mg/dl), aspirin reduced serum Lp(a) levels to approximately 80 % of the baseline after one month. Their levels sustained significantly low even after six months. The effect of aspirin in reducing elevated serum Lp(a) levels were stronger in patients with smaller-sized type or double-band type of apo(a) isoforms. The transcriptional efficiency of apo(a) gene is thought to be increased in patients with these apo(a) isoforms. Therefore, these findings suggest that aspirin reduces apo(a) gene transcription preferentialy in patients with high transcriptional efficiency of this gene

Retinal Dysfunction and Progressive Retinal Cell Death in SOD1-Deficient Mice

The superoxide dismutase (SOD) family is a major antioxidant system, and deficiency of Cu,Zn-superoxide dismutase (SOD1) in mice leads to many different phenotypes that resemble accelerated aging. The purpose of this study was to examine the morphology and physiology of the sensory retina in Sod1−/− mice. The amplitudes of the a- and b-waves of electroretinograms elicited by stimuli of different intensity were reduced in senescent Sod1−/− mice, and this reduction in amplitude was more pronounced with increasing age. Retinal morphometric analyses showed a reduced number of nuclei in both the inner nuclear cell layer and outer nuclear cell layer. Electron microscopy revealed swollen cells and degenerated mitochondria in the inner nuclear cell and outer nuclear cell layer of senescent Sod1−/− mice indicating necrotic cell death. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling revealed no significant differences in the number of apoptotic cells between Sod1−/− and wild-type mice, and activated caspase-3 could not be detected in the retina of Sod1−/− mice. In addition to the age-related macular degeneration-like phenotypes previously reported, Sod1−/− mice also present progressive retinal degeneration. Our results indicate that Sod1−/− mice may be a good model system in which to study the mechanism of reactive oxygen species-mediated retinal degeneration