Fiberoptic evaluation of peripheral airways of two patients with acute respiratory failure during mechanical ventilation.
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Biomedical subjects
Publications and source records attributed to M Shimada.
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An expression of desmosomal glycoprotein 1 (DG 1) was immunohistochemically examined in 77 biopsies and 21 metastatic cervical lymph nodes of oral squamous cell carcinomas (SCC). In the primary tumors the DG 1 expression was significantly reduced at the invasive site of poorly differentiated and highly invasive tumors. In cases of metastases in cervical lymph nodes, the DG 1 staining at the invasive site of the primary tumor was significantly less than that of nonmetastatic cases. The DG 1 expression in the metastatic lymph nodes was as weak as that in the primary tumor. Thus, we suggest that immunohistochemical investigation of DG 1 expression in oral SCC is valuable in predicting tumor behavior.
A 2830 g full-term baby, born by breech delivery, exhibited weak crying and sucking and severe hypotonia of the extremities after birth. Magnetic resonance imaging (MRI) showed marked thinning of the cervical cord at the level of C4 and C5. This lesion evolved into focal syringomyelia by the fourth month after birth. In this patient, MRI was useful in detecting the initial spinal cord injury, which appeared as marked thinning, and the subsequent syringomyelia as well. The role of birth trauma in cervical spinal cord injuries is discussed.
The development of an antiomony electrode (Sb) and a pH meter as a substitute for a glass electrode(G) to measure the intramyocardial pH is reported, and the results of their clinical application. The determination of the pH of CPD (citrate-phosphate-dextrose) blood by Sb showed small differences when compared to G (less than 0.1). Sb was also temperature sensitive. The temperature coefficient of Sb was determined in buffers by varying their temperatures, and an antimony-thermocouple electrode and a temperature-compensated pH meter were subsequently constructed. In CPD blood of varying temperatures Sb showed similar tendencies to G. The results of the application of the new apparatus to 28 patients were statistically no different from those obtained previously by G on 22 patients, either in baseline pH or its fall following aortic cross-clamping. It is concluded that although Sb is not as accurate as G, it is a reasonable alternative for the determination of myocardial acidosis during open-heart surgery.
Respiratory induced changes in superior (QSVC) and inferior (QIVC) vena caval flows and abdominal pressures were evaluated in anesthetized closed-chest dogs. QSVC and QIVC were measured with ultrasound transit time flow probes (n = 5), and general (Pab) and regional subdiaphragmatic (Pd) abdominal pressures were measured by air-filled balloons (n = 5), during two respiratory maneuvers produced by phrenic nerve stimulation, i.e., simulated spontaneous inspiration (SSI), and Mueller maneuver (MM), with the airway occluded to minimize diaphragmatic descent. With hypervolemia: during SSI, QSVC decreased, QIVC increased, and right atrial pressure increased (P less than 0.05) despite a decrease in esophageal pressure (Pes), i.e., Kussmaul's sign; during MM, both QSVC and QIVC increased (P less than 0.05) without Kussmaul's sign. The ratios delta Pab/delta Pes and delta Pd/Pes were larger during SSI than MM (P less than 0.01). With hypovolemia: during SSI and MM, QSVC increased and QIVC decreased with a venous pressure gradient across the diaphragm (P less than 0.05), consistent with development of a vascular waterfall. These results suggest that 1) changes in abdominal pressure may affect the patterns of QSVC and QIVC during respiration, depending on blood volume status; 2) a prolonged inspiration with hypovolemia may decrease QIVC because of the development of a vascular waterfall; 3) QSVC and QIVC may be interdependent during respiration; and 4) the essential mechanism of Kussmaul's sign is a substantially larger inspiratory increase in abdominal pressures produced by diaphragmatic descent compared with the decrease in intrathoracic pressure under hypervolemic conditions, rather than the presence of pericardial pathology or right heart dysfunction.
The effects of the pericardial constraint in control, tamponade, and absent pericardium conditions was studied in 18 anesthetized open-chest dogs. Atrial pressures and systolic and diastolic inflow volumes per beat in the superior (SVC), inferior vena cavae (IVC), and pulmonary vein (PV) were measured. With increasing tamponade, 1) the systolic-diastolic distribution of venous flow became almost exclusively systolic in the SVC (P less than 0.001) and IVC (P less than 0.05), as the gamma-descent disappeared; 2) similar but lesser left-sided changes occurred in PV flows (P less than 0.001) and pressure; and 3) the systolic-diastolic distribution of venous flow was modulated by heart rate. The results imply that during tamponade 1) increased pericardial liquid pressure associated with an increased pericardial constraint couples reciprocal atrial and ventricular volume changes; 2) the atria fill during ventricular ejection (atrioventricular interaction); 3) total heart volume must have been relatively constant throughout a cardiac cycle; and 4) differences in right and left heart compliances may explain persistent diastolic PV flow. Pericardiotomy produced a small increase in the ratio of diastolic to systolic venous inflow volumes (P less than 0.025), suggesting that normally the pericardium has a minor influence on atrioventricular interaction, the volume changes in the atria and ventricles being relatively uncoupled. With severe tamponade, a homogeneous pericardial fluid column tightly couples atrial and ventricular volume changes and accounts for the characteristic changes in atrial pressure waveforms and patterns of venous flow.
Apo E plays an important role in plasma lipoprotein metabolism through its high affinity binding to cell surface LDL receptor. In the present study, we studied the effects of apo E on the atherogenic process in Watanabe heritable hyperlipidemic rabbits which are deficient in LDL receptor and an animal model for familial hypercholesterolemia. We isolated apo E from plasma of 1% cholesterol-fed rabbits and administered 10 mg of purified apo E intravenously into five Watanabe heritable hyperlipidemic rabbits three times a week from their age of 2.5 months to 11 months for 8.5 months. After sustained administration to apo E, we found a significant reduction in the accumulation of cholesterol ester in aortae (1.55 +/- 0.07 mg/g tissue) as compared to control rabbits (4.32 +/- 0.61 mg/g tissue). Supporting this, the percentage of the surface area of the aorta with macroscopic plaque was remarkably decreased in apo E-treated animals (18.8 +/- 5.1% vs. 38.8 +/- 8.0% in control). Thus, apo E definitely prevented the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbits.
We have reported that transgenic mice overexpressing rat apo E shows marked reduction of plasma cholesterol and triglyceride levels due to the disappearance of VLDL and LDL. In this study, we investigated the metabolism of plasma lipoproteins in transgenic mice. After intravenous injection, the rates of clearance of 125I-VLDL and 125I-LDL were 3.0- and 2.4-fold greater in transgenic mice than in controls, respectively. Furthermore, clearance of chylomicron remnants estimated by oral retinyl palmitate-loading test was markedly enhanced in transgenic mice. The hepatic expression of LDL receptors by immunoblot analysis was similar in both groups. These data suggest that elimination of lipoproteins containing apo B was due to enhanced clearance of these lipoproteins enriched with apo E through hepatic LDL receptors. When fed a high cholesterol diet, controls showed twofold elevation of plasma cholesterol levels with marked increases in VLDL and LDL cholesterol on gel filtration chromatography. In contrast, cholesterol-fed transgenic mice showed resistance against these increases. High cholesterol feeding decreased the activity of hepatic LDL receptors and had no effect on enhancement of chylomicron remnant clearance in transgenic mice. Thus, overexpression of apo E facilitates metabolism of lipoproteins containing apo B presumably primarily via the LDL receptor pathway and possibly through an interaction with the chylomicron remnant receptor.
The distribution of insulin binding sites in the mouse was investigated by in vivo whole-body autoradiography. Male mice were injected intravenously with 125I-insulin in the absence of and, in the presence of, excess unlabeled insulin. Three, 6, 15, 30 and 60 minutes after injection, the animals were perfused and subjected to autoradiographic procedures. Specific insulin binding was observed in the choroid plexus, liver, gastrointestinal tract, spleen, pancreas, deferent duct, and Harderian gland. In the liver and spleen, the distribution of binding sites was heterogeneous. In the liver, the density of the binding was higher around the branches of the portal vein than around the central vein. In the spleen, the marginal zone exhibited a higher density than the white and red pulp. The kidney cortex, and the thyroid gland showed a high degree of insulin binding, but the binding was nonspecific. The binding of insulin to other tissues and organs, including the skeletal muscle and fat, was weak, and most of the binding was nonspecific.
Recently, we reported that human monocyte colony-stimulating factor (M-CSF) stimulates the clearance of lipoproteins containing apoB100 via both low density lipoprotein receptor-dependent and -independent pathways in target cells of M-CSF, and reduces plasma cholesterol level (Journal of Biological Chemistry, 265:12869-12875, 1990). This suggests a linkage of cytokines to the metabolic regulation of plasma cholesterol. Furthermore, we found a significant role of M-CSF in cholesterol metabolism of human monocyte-derived macrophages. M-CSF enhanced not only the uptake of acetylated low density lipoprotein and oxidized low density lipoprotein in macrophages, but also the efflux of cholesterol from cholesterol-loaded macrophages. To elucidate in vivo effects of M-CSF on cholesterol efflux from tissues, we administered an intravenous injection of 3H-cholesterol (150 microCi) into WHHL rabbits 1 month before starting M-CSF treatment. We observed an increased cholesterol efflux from tissues to plasma high density lipoprotein after M-CSF treatment when cholesterol efflux was estimated as the change in specific radioactivity of plasma high density lipoprotein-cholesterol. This result suggests that M-CSF can enhance the excretion of cholesterol from target cells of M-CSF, such as cholesterol-loaded macrophages in the arterial wall, and reduce the rate of atherogenesis.
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A rapid detection method was developed for DNA polymorphisms in the human lipoprotein lipase (LPL) gene. The examined polymorphisms include an A-C transversion in the 5'-region of intron 3, a T-G transversion that occurs within a Hind III site of intron 8, and the previously described C-T transition that causes a Pvu II polymorphism in intron 6. Gene fragments encompassing each polymorphic site were amplified by the polymerase chain reaction (PCR) and digested with an appropriate restriction enzyme whose recognition site was either naturally affected by the polymorphism or artificially created with a mismatched PCR-primer. According to the digestion profiles, genotypes were unambiguously distinguished. With this method, respective allelic frequencies were determined for 50 or 70 normal subjects. The procedure will facilitate LPL genotyping in the large population.
Effect of pretreatment of rats with FK506((-)-(1R,9S,12S,13R,14S,17R,18E,21S,23S,24R,25S,27R)-17-allyl-1,14- dihydroxy-12-[(E)-2-[(1R,3R,4R)-4-hydroxy-3methoxycyclohexyl]-1- methylvinyl]-23,25-dimethoxy-13,19,21,27-tetramethyl-11,28-dioxa-4- azatricyclo-[22.3.1.0(4.9)]octacos-18-ene-2,3,10,16-tetrone hydrate, CAS 104987-11-3) on microsomal cytochrome P-450 system and oxidations of the administered drug and other model substrates were studied and compared with those of a pharmacologically related drug, ciclosporin (cyclosporin A). Oral treatment of male Sprague-Dawley rats with FK506 (0.4, 2 or 10 mg/kg/d) for 7 days did not decrease microsomal content of total cytochrome P-450 in livers, but rather increased the content in groups with the dose of 0.4 or 10 mg/kg to the levels of 126-130% of the control. Microsomal NADPH-cytochrome c reductase activities were decreased up to 67% of the control with the increasing dose of FK506 and to 62% in a group treated orally with cyclosporin A (25 mg/kg/d for 7 days), although another microsomal electron-transport component, cytochrome b5, was rather increased in all the treated groups. Treatment with FK506 or cyclosporin A did not reduce but slightly increased microsomal activities of aniline hydroxylation, p-nitroanisole O-demethylation and O-ethoxyresorufin O-deethylation. Microsomal depropylation of 7-propoxycoumarin, a typical P-450IIIA-substrate, was also not reduced in all dose groups of FK506, while it was decreased by the treatment with 25 mg/kg cyclosporin A.(ABSTRACT TRUNCATED AT 250 WORDS)
Histopathological features of the lymph node involvement were studied in 104 patients with thoracic esophageal cancer who underwent subtotal esophagectomy combined with extended radical lymph adenectomy in cervicothoracoabdominal region. Metastatic involvement was found in a total number of 503 lymph nodes from 73 patients by histologic examination. The mean of long and short diameter was found to be less than 5mm in 125 (24.9%) of these 503 nodes. The involved area on the section was less than one third in 149 nodes (29.6%), and was significantly smaller in mediastinal lymph nodes than those in cervical or abdominal ones. Sixty-seven (13.3%) of 503 nodes were partially invaded by micrometastasis of 1mm or less in diameter. Micrometastasis also more frequently occurred in mediastinal nodes with a statistically significant difference. Extranodal proliferation (ENP) of cancer cells was found in 106 nodes (21.1%), and extranodal lymphatic and/or blood vessel invasion (ENly, v) was also recognized in 60 nodes (11.9%). Micrometastasis and ENP with or without ENly, v were found in 24 (32.9%) and 29 (39.7%) of 73 patients with positive lymph node metastasis, respectively. Postoperative survival rate in patients with micrometastasis and/or ENP with or without ENly, v was inferior to that in patients with neither of them.
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In order to study the factors responsible for glucose uptake in the mouse hippocampus, microvessel and astroglial cell densities were measured and compared in each laminal region. Microvessel density was examined on histologically prepared sections after injection of Indian ink and measured by means of an image analyser. Astroglial cell density was determined after the cells were stained immunohistochemically. Microvessel and astroglial cell densities were determined in 10 different hippocampal structures. Microvessel and astroglial cell densities were strongly correlated in all layers except the pyramidal cell layers. The highest density of perfused microvessels was found in the stratum lacunosum-moleculare, compared with other regions, and the lowest values were found in the stratum lucidum and dentate granular cell layer. Among pyramidal cell layers, microvessel density in sector CA3a was significantly higher than that in CA1.
A quantitative analysis of small pulmonary arteries, pulmonary veins, and lymphatic vessels was conducted in autopsy cases of total anomalous pulmonary venous connection. The materials were obtained from 60 cases of total anomalous pulmonary venous connection without asplenia or pulmonary stenosis, ages ranging from 2 days to 19 months at the time of death (mean age 2.2 months). Pulmonary arterial pressure had been measured in 32 of these patients before death. Twenty cases of ventricular septal defect with pulmonary hypertension and 15 normal individuals were used as the control group. The mean thickness of the media of small pulmonary arteries and veins was 12.7 and 7.6 microns, respectively, in the total anomalous pulmonary venous connection cases, both values being significantly larger than those for normal and ventricular septal defect cases. No changes in thickness with aging were found. Medial thickness in the arteries and veins was greater in the cases of pulmonary venous obstruction than in those without such obstruction. The medial thickness of small pulmonary arteries in total anomalous pulmonary venous connection cases correlated with increased pulmonary arterial pressure. When the patients with the same pulmonary arterial pressure levels were compared, the medial thickness was always greater in those who had total anomalous pulmonary venous connection than in those who had ventricular septal defect. The medial thickness of pulmonary veins was also highly correlated with increased pulmonary arterial pressure in total anomalous pulmonary venous connection. The severity of the intimal lesions was milder in those who had total anomalous pulmonary venous connection than in those who had ventricular septal defect, suggesting the protective role of the thickened pulmonary arterial media against development of intimal lesions. Intimal fibrous thickening of pulmonary veins was not seen in the cases of ventricular septal defect, but it was present in 45% of the total anomalous pulmonary venous connection cases. Lymphangiectasia was characteristically present in 62% of the total anomalous pulmonary venous connection cases. Interstitial emphysema was often a complication of lymphangiectasia, and it led to eight postoperative deaths.
Our recent experiences of the autogenous pericardial patch augmentation of Blalock-Taussig anastomotic orifice are reported. In Case 1, the direct suture between the left subclavian artery and the left pulmonary artery was difficult on the anterior wall because of the shortness of the left subclavian artery. Therefore, a piece of the patient's own pericardium was excised and sutured anteriorly between the two vessels by interrupted 7-0 polypropylene sutures. A 19 months postoperative angiogram showed so-called parrot-beaking of the subclavian artery probably due to tension, but there was no distortion or stenosis of the pulmonary artery. In Case 2, the right subclavian artery distal to the bifurcation of the vertebral artery was longitudinally split measuring approximately 2.5 cm in length, and widened by a piece of the autogenous pericardium in a wedge shape. Then, it was anastomosed to the right pulmonary artery without undue tension. Seven months postoperatively the patient died from severe AV valve regurgitation. The autopsy showed widely patent anastomosis and good healing as well as slight expansion of the pericardial patch but without aneurysm formation. In Case 3, the same operation as in Case 2 was performed. A 6 months postoperative angiogram showed no stenosis or distortion of either the subclavian or the pulmonary artery. Although it is premature to draw any conclusion, the use of the autogenous pericardium may be indicated to widen the anastomotic orifice of Blalock-Taussig shunt without sacrificing the length of the subclavian artery even in small infants or neonates.