Simple, rapid and automated method for detection of hyperaggregability of platelets in sleep apnea syndrome.
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Biomedical subjects
Publications and source records attributed to K Kamio.
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The incidences of cardiovascular and cerebrovascular diseases are reportedly higher in patients with obstructive sleep apnea (OSA) than in OSA-free subjects, though the mechanism remains unknown. Recently, the contribution of activated platelets to a number of pathological conditions such as stroke or ischemic heart disease has been suggested. We hypothesized that the expression of activated platelet markers resulting from OSA might be higher than in healthy subjects. By flow cytometry using monoclonal antibodies, we measured two such markers, PAC-1 and CD 62 P, in OSA patients and healthy subjects. Twelve healthy men (age, 52.7 +/- 12.8 y/o; and body mass index (BMI), 22.2 +/- 16.1 kg/m2; mean +/- S.D.) and 20 male patients with OSA (age, 50 +/- 7.96 y/o; BMI, 28.1 +/- 3.3 kg/m2; apnea hypopnea index (AHI), 38.2 +/- 21.2 times/hr; and lowest SpO2, 75.6 +/- 11.3%) were enrolled in this study. PAC-1 expression was significantly higher in OSA patients (65.1 +/- 17.8%) than in healthy subjects (16.8 +/- 7.4%), as was CD 62 P expression (8.5 +/- 8.8% vs. 0.88 +/- 0.57%). The increase in PAC-1 expression was correlated with AHI and the arousal index. These findings suggest that activated platelet markers could be good indicators for untreated OSA.
We encountered a case of crescent-type tracheobronchomalacia in a 54-year-old male smoker. The patient experienced extreme obstructive pulmonary changes but his FVC and DLco findings were within the normal ranges. Plain chest X-ray films indicated tracheal narrowing, a diagnosis that was confirmed by fiberoptic bronchoscopy. Two Z-stents were implanted in the trachea but the patient's symptoms did not subside. Thoracic computed tomography (CT) elucidated stenosis of both main bronchi at end-expiration. The implantation of Z-stents in the main bronchi remarkably alleviated the symptoms and improved peak expiratory flow. Six months after implantation, the tracheal stents broke. A favorable course was obtained by inserting an ultraflex stent inside the broken Z-stents. DLco is important to the diagnosis of tracheobronchomalacia, whereas peak expiratory flow and thoracic CT findings are useful in evaluating the effectiveness of treatment. We concluded that ultraflex stents should be the first choice for treatment of tracheal stenosis, and that Z-stents are appropriate for the treatment of bronchial obstruction.
A 44-year-old woman who had been treated for bronchial asthma for 5 years was admitted for further evaluation of progressive dyspnea. Physical examination revealed wheezing originating in the neck. A flow-volume curve suggested upper-airway stenosis. The patient had no history of trauma, endotracheal intubation, granulomatous diseases, or any other severe respiratory tract infections. Chest radiography and laboratory examination showed no abnormalities. Tracheal X-P, computed tomography and magnetic resonance imaging of the neck, and bronchoscopy demonstrated circumferential subglottic tracheal stenosis extending for 40 mm. The diameter of the lumen was 5 mm at its narrowest. The trachea distal to the lesion was normal. Bronchoscopic biopsy revealed thickened tracheal mucosa and submucosa with increased fibrous tissue and chronic inflammatory cell infiltration, suggesting a nonspecific inflammatory process. These findings are compatible with idiopathic tracheal stenosis, which was reported by Bhalla et al. The patient was treated with Nd-YAG laser surgery via a fiberoptic bronchoscope, which resulted in a great improvement in respiration. Regression of the lesion has not occurred in the 40 months since the laser surgery. The majority of patients with this condition have been treated by surgical resection of the stenotic lesion and reconstruction. However, the success of Nd-YAG laser surgery in the present case suggests that this approach would be a satisfactory alternative procedure for treatment of idiopathic tracheal stenosis.
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We report 7 patients with severe acute asthma unresponsive to standard medication, including sympathomimetic agents, aminophylline and corticosteroids, who responded to inhaled frusemide. All were hypercapneic with a mean PaCO2 of 7.7 kPa (57.7 mm Hg) [range 6.2-8.8 kPa (46.2-66.3 mm Hg)]. Following nebulization of 20 mg frusemide, clinical response was rapid, and the mean PaCO2 fell significantly to 5.4 kPa (40.6 mm Hg) [range 5.0-6.2 kPa (37.5-46.5 mm Hg)] within 20-60 min. No adverse effect was recognized. Inhaled frusemide should be considered for treatment of acute asthma refractory to conventional therapy.
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In the course of characterization of glycolipid sulfotransferase from human renal cancer cells, the manner of inhibition of sulfotransferase activity with pyridoxal 5'-phosphate was investigated. Incubation of a partially purified sulfotransferase preparation with pyridoxal 5'-phosphate followed by reduction with NaBH4 resulted in an irreversible inactivation of the enzyme. When adenosine 3'-phosphate 5'-phosphosulfate was coincubated with pyridoxal 5'-phosphate, the enzyme was protected against this inactivation. Furthermore, pyridoxal 5'-phosphate was found to behave as a competitive inhibitor with respect to adenosine 3'-phosphate 5'-phosphosulfate with a Ki value of 287 microM. These results suggest that pyridoxal 5'-phosphate modified a lysine residue in the adenosine 3'-phosphate 5'-phosphosulfate-recognizing site of the sulfotransferase.
Asthmatic patients are sometimes ignorant of their treatment and of the pathophysiology of their disease. In such patients, anxiety about the disease may worsen their condition. We studied the effects of an educational program for bronchial asthma. In 45 patients, the Severity of Asthma Scores before and after the program were measured. Sixty percent of the patients were assessed as "improved". On self-administered questionnaires concerned with asthma, most of the patients indicated that the program significantly improved their condition, reduced apprehension about the disease, and increased their trust in the hospital. In 24 patients, three psychological tests were done. Results of the comprehensive asthma inventory indicated that the program was useful for dependent and self-disciplined patients, but was not useful for resigned and depressed patients. The Y-G test showed that most of the patients who were helped by the program were introverted. Results of the Edwards Personal Preference Schedule revealed a difference in desire between the group that benefitted from the program and the group that did not. These results suggest that each group had a certain inclination toward psychogenic symptoms. Therefore, psychological tests are useful for predicting the effects of education. In conclusion, educational programs for patients with bronchial asthma may affect morbidity from asthma. Possible mechanisms include relief of anxiety about the disease and improvement in the patient's compliance with prescribed therapy.
OBJECTIVE: To identify phenotypic characteristics of a certain mutation in the peripherin/RDS gene. DESIGN: Case reports with clinical features and results of fluorescein angiography, electroretinography, kinetic visual field testing, dark adaptometry, and DNA analysis. SETTING: University medical center. PATIENTS: We studied the ocular findings in eight members of a Japanese family with autosomal dominant retinitis pigmentosa and cytosine-to-adenine transversion at the third nucleotide in codon 244 of the peripherin/RDS gene. This mutation resulted in a substitution of lysine for asparagine in amino acid 244 of peripherin/RDS, a photoreceptor-specific glycoprotein. RESULTS: Clinical findings of each affected member in this family showed a marked intrafamilial similarity, which may provide the natural course of the phenotype produced by the Asn244Lys mutation. Characteristic features include diffuse pigmentary retinal degeneration in the midperipheral and peripheral fundi associated with macular degeneration in the later stage, starting with bull's-eye maculopathy, and severely deteriorated electroretinographic findings in both rods and cones, even in the early stage. CONCLUSION: The mutation at codon 244 of the peripherin/RDS gene causes both rod and cone degeneration, although the precise mechanism of retinal degeneration is currently unknown.
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The cDNA encoding adenovirus E1A enhancer-binding protein E1A-F was isolated by screening a HeLa cell lambda gt11 expression library for E1A-F site-specific DNA binding. One cDNA clone produced recombinant E1A-F protein with the same DNA binding specificity as that endogenous to HeLa cells. Sequence analysis of the cDNA showed homology with the ETS-domain, a region required for sequence-specific DNA binding and common to all ets oncogene members. Analysis of the longest cDNA revealed about a 94% identity in amino acids between human E1A-F and mouse PEA3 (polyomavirus enhancer activator 3), a recently characterized ets oncogene member. E1A-F was encoded by a 2.5kb mRNA in HeLa cells, which was found to increase during the early period of adenovirus infection. In contrast, ets-2 mRNA was significantly reduced in infected HeLa cells. The results indicate that E1A enhancer binding protein E1A-F is a member of the ets oncogene family and is probably a human homologue of mouse PEA3.
A cell line (SMKT-R3) established from human renal cell carcinoma was characterized for the presence of sulfolipids and glycolipid sulfotransferases. Sulfolipids were found to constitute a large part of the acidic glycolipid fraction in SMKT-R3 cells. These findings were confirmed by metabolic labelling with 35S-sulfate. These sulfolipids were expressed at the surface of SMKT-R3 cells as ascertained by cytofluorometry using a monoclonal antibody directed to sulfolipids. Furthermore, markedly high activity levels of glycolipid sulfotransferases were observed in SMKT-R3 cells compared with other cell lines. These results suggest that the increased synthesis of sulfolipids in renal cell carcinoma tissue (Sakakibara et al., 1989. Cancer Res., 49, 335-339) is due to the elevation of the sulfotransferase activities of renal carcinoma cells themselves.
It remains unknown how increased upper airway resistance (UAR) during sleep could be a function of gravity. We therefore conducted quantitative evaluation of the gravitational influence on diaphragmatic EMG activity (EMGdi) in an astronaut to estimate the effect of UAR in space. EMGdi was recorded by paired surface electrodes on the ground (control, C) and abroad a short-term space mission (space, S) for 30 consecutive h. Mean EMGdi recorded during quiet breathing in wakefulness was assigned the value of 100. EMGdi in C was significantly enhanced in all sleep stages compared with that while awake in the supine position (mean +/- SD, 230 +/- 23.2% in non-rapid eye movement (non-REM) Stage II, 233 +/- 13.8 in slow-wave sleep, and 233 +/- 40.0 in REM sleep versus 100 +/- 17.3 in wakefulness, p < 0.001). In contrast, there was no statistical difference in EMGdi in S between awake and any non-REM sleep stage (mean +/- SD, 100 +/- 20.5% in wakefulness versus 103 +/- 16.9 in non-REM Stage II and 100 +/- 14.8 in slow-wave sleep; NS). However, EMGdi in REM sleep in S was statistically greater (132 +/- 28.3%) than that during wakefulness or any other sleep stage in space (p < 0.001). Therefore, gravity may play a much more significant role in the normal healthy human in the increased upper airway resistance during sleep than the relative atonia of the upper airway muscles.
We report a 71-year-old female patient with primary alveolar hypoventilation syndrome who received diaphragm pacing (DP) and developed obstructive sleep apnea syndrome (OSAS). Application of nCPAP markedly improved her nocturnal hypoxemia. The monitored polygrams before and after the application strongly suggested that the main mechanism of OSAS was an imbalance of activity between upper airway dilator muscles and pump muscles. Moreover, paradoxical movement of the rib cage is not necessarily due to upper airway obstruction. Monitoring of tidal volume and arterial oxygen saturation is essential for the diagnosis of DP-induced OSAS.
Glycolipid sulfotransferase activity in human and rat hepatocellular carcinoma tissues was studied, since an elevated level of the enzyme activity in serum had been demonstrated in cancer patients. The level of the enzyme activity in carcinoma tissues, however, could not be distinguished from that of normal controls. Similar observations were made for rat hepatoma. A higher level of enzyme activity was observed in the female than in the male. Inconsistent expression between hepatoma tissue and serum suggests that humoral factor(s) derived from hepatoma tissue stimulates production of the sulfotransferase, which is released into the blood-stream in the host.