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Biomedical subjects

M Yonemaru

Publications and source records attributed to M Yonemaru.

At least 37 records · Page 2Linked to original sources

[An autopsy case of lymphoepithelioma-like carcinoma of the mediastinum].

A case of lymphoepithelioma-like carcinoma of the mediastinum is reported. A 67-year-old male was admitted to Tokyo Medical College Hospital, in February of 1992, for evaluation of an abnormal mediastinal shadow on chest X-ray. The mediastinal tumor was biopsied using mediastinoscopy. Histological diagnosis was undifferentiated carcinoma and radiation therapy was performed. Six months after treatment, he complained of dyspnea. Combination chemotherapy was performed. Although the tumor size decreased, he died of pneumonia. Histological findings at autopsy included nesting of large carcinoma cells with vacuolar nuclei and large nucleoli, interstitial lymphocytic infiltration similar to that of lymphoepithelioma of the epipharynx, and lymphoepithelioma-like carcinoma in the thymus. The epipharynx and thymus were, however, intact at autopsy. We found no other origins of this tumor, including the trachea and lung. This case was therefore diagnosed as lymphoepithelioma-like carcinoma of the mediastinum.

Aged↗

[Diagnosis of B-cell lymphoma of lung by kappa-lambda imaging in broncho-alveolar lavage fluid lymphocytes].

We attempted to verify the clonality of proliferating cells in broncho-alveolar lavage fluid (BALF) by using a sophisticated technique known as kappa-lambda imaging. We applied this method to BALF lymphocytes from 3 cases suspected of having primary pulmonary B-cell lymphoma, by transbronchial lung biopsy, and from 2 cases with B-cell lymphoma revealing abnormal shadows. (One was diagnosed as small cell carcinoma, the other mycotic infection). B-cell monoclonality was found in the former 3 cases, but not in the latter 2 cases. We conclude that kappa-lambda imaging in BALF lymphocytes is useful for diagnosing B-cell lymphoma of the lung.

Aged↗

[A case of pulmonary fibrosis associated with CMV inclusion body].

A 71-year-old woman admitted to our hospital with complaints of progressive dyspnea on exertion and weight loss. Roentgenological examination demonstrated peripheral pulmonary fibrosis and a mediastinal tumor suggesting thymoma. The pathological findings of transbronchial lung biopsy (TBLB) confirmed pulmonary fibrosis. Moreover, cytomegalic inclusion bodies in TBLB and a high titer of serum CMV IgG antibody suggested pulmonary CMV infection. It is considered that pulmonary fibrosis and CMV infection were coexistent in this patient.

Aged↗

Detection of tracheal stenosis by frequency analysis of tracheal sounds.

To develop a simple noninvasive method for detecting tracheal stenosis, tracheal sounds were analyzed using fast-Fourier transform. The subjects were all female and included 5 normal volunteers and 13 patients with tracheal stenosis mostly secondary to thyroid cancer (11 extrathoracic and 2 intrathoracic lesions). Tracheal sounds were recorded during spontaneous breathing and were digitized with an analog-to-digital converter. Pulmonary functions, including forced expiratory volume in 1 s (FEV1) expressed as percentage of vital capacity, peak expiratory flow rate (PEFR), the ratio of FEV1 to PEFR (Empey's index), and the ratio of expiratory to inspiratory flow rates at 50% vital capacity, were measured. A computed tomography scan was used to obtain the tracheal minimum cross-sectional area. Whereas PEFR demonstrated a weak correlation with the stenotic area, FEV1%, Empey's index, and the ratio of expiratory to inspiratory flow rates at 50% vital capacity did not. The power of the fast-Fourier transform spectrum of normal tracheal sounds decreased as the frequency increased up to 500 Hz. A small spectral peak was observed at approximately 1 kHz. Patients with significant tracheal stenosis demonstrated an increase in the peak spectral power at approximately 1 kHz and in the mean spectral power from 600 to 1,300 Hz in their tracheal sounds. In patients with extrathoracic lesions, the peak and mean spectral powers correlated well with the area of the stenosis as defined by computed tomography scan. In patients with intrathoracic lesions, abnormalities in the pulmonary functions as well as tracheal sound spectra appeared more evident despite milder stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Early detection of chronic obstructive pulmonary disease by following individual annual changes in lung function].

The possibility of early detection of chronic obstructive pulmonary disease (COPD) was investigated among subjects whose lung function could be followed for more than ten years. Ten subjects aged 60 or more were selected from among about 1500 cases using the following diagnostic criteria; (1) subjects had complained of exertional dyspnea (2) chest X-ray abnormalities were suggestive of COPD (3) FEV1.0% was under 55%. Data on FVC/height, FEV1.0/height and FEV1.0% of these subjects were available for the previous ten years. Individual linear regression equations were estimated. Average annual changes of cases of obstruction were compared with those of normal cases, and individual deviations from the normal standard range were observed. Declines of the regression lines were as follows; FEV1.0/height: normal case--0.016 +/- 0.017, obstruction cases--0.038 +/- 0.018 (L/m/yr), FEV1.0%: normal cases 0.164 +/- 0.627, obstruction cases--1.522 +/- 0.638 (%/yr). Significant differences were observed between the normal and the obstruction cases (p < 0.01). FEV1.0% of all obstruction cases was under--2 SD of that of normal subjects. All individual FEV1.0% regression lines of the obstruction cases were outside +/- 2 RSD of the normal standard range more than 5 years before the onset of symptoms. Following individual annual changes in lung function was considered to be useful for the early detection of COPD.

Adult↗

[Effects of inhibitors of intracellular signal transduction on lipopolysaccharide-induced increase in permeability of cultured pulmonary endothelial cell monolayers].

To investigate the mechanism of lipopolysaccharide (LPS)-induced endothelial response, we measured the permeability to albumin of cultured pulmonary endothelial cell monolayers. PMA and SC-9, used as activators for protein kinase C (PCK), failed to cause an increase in permeability to albumin. H-7, a potent PKC inhibitor, did not prevent the LPS-induced increase in permeability to albumin. In contrast, H-8, which strongly inhibits cyclic nucleotide-dependent protein kinases, and a calmodulin antagonist prevented the LPS-induced increase in permeability to albumin. These results suggest that calmodulin and protein kinases other than PCK are implicated in the mechanism of LPS-induced increase in permeability to albumin.

Albumins↗

[Determination of pulmonary blood flow by acetylene rebreathing method in patients with chronic respiratory disease].

Non-invasive measurement of pulmonary blood flow by acetylene rebreathing was performed in patients with pulmonary diseases. Cardiac output measurement by thermodilution method was also used simultaneously. A fast computation system was coupled with the measurement. Fourteen emphysema patients and 7 pulmonary fibrosis patients were the subjects. Ten patients with normal lung function were normal controls. After the measurement of cardiac output, the subjects rebreathed mixed gas containing acetylene and argon from the end tidal level. The inspiratory and expiratory gas was measured by mass-spectrometer. A lung model made of two compartments connected in series, a compartment of the rebreathing bag and a compartment of the lung were used for the analysis, while taking account of the volume reduction due to O2 and CO2 exchange and the fluctuation of end tidal gas concentration until equilibrium between the bag and the lung was reached. Values in 9 emphysema cases and 6 fibrosis cases were within or near the 90% confidence limits of control. Five emphysema cases were obviously out of the range, and their pulmonary blood flow was less than the cardiac output and their mean arterial PCO2 was higher than that of the other emphysema cases. These cases were considered to have blood flow to the sites with low alveolar ventilation per unit volume.

Acetylcholine↗

Atriopeptin-induced increases in endothelial cell permeability are associated with elevated cGMP levels.

To investigate the mechanism of nonrenal capillary hyperfiltration, we studied the effect of atriopeptin (AP) III and AP I on permeability and intracellular cyclic nucleotide levels in cultured bovine pulmonary artery endothelial cell monolayers. Permeability to albumin was assessed by the albumin transfer rate across endothelial cell monolayers, following a 4-h incubation with atriopeptins. AP III (0.01, 0.1, and 1 microM) caused a concentration-dependent increase in the albumin transfer rate. AP III induced a threefold increase in intracellular guanosine 3',5'-cyclic monophosphate (cGMP) levels during the incubation period. A phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), enhanced the AP III-induced increase in permeability and cGMP accumulation by 16-fold at maximum. 8-Bromoguanosine 3',5'-cyclic monophosphate, a hydrolysis-resistant cGMP analogue, caused a slight but significant increase in permeability. In contrast, AP I, a weak agonist of the cGMP-coupled ANP receptor, did not elicit an increase in permeability at concentrations of 0.1 and 1 microM. Although AP I (1 microM) caused a significant increase in cGMP by 33 and 60% in the absence and presence of IBMX, the increase was markedly less compared with AP III. AP III did not cause a change in intracellular cAMP levels during the incubation period. These observations suggest that in our system AP III increases the permeability of endothelial cell monolayers in association with an elevated cGMP level. Thus an increase in permeability might be involved in the mechanism of ANP-induced capillary hyperfiltration.

Animals↗

Hilar and mediastinal lymphadenopathy with hypersensitivity pneumonitis induced by penicillin.

A 54-year-old Japanese man demonstrated a sultamicillin-induced hilar and mediastinal lymphadenopathy with hypersensitivity pneumonitis. A positive lymphocyte stimulation test for sultamicillin and a decreased CD4/CD8 ratio of lymphocytes in BAL fluid suggested that an alteration in cell-mediated mechanisms was responsible for the patient's symptoms.

Alveolitis, Extrinsic Allergic↗

[Pulmonary blood flow measurement by acetylene rebreathing method in subjects without respiratory function disturbance].

Simultaneous measurement of pulmonary blood flow by the acetylene rebreathing method and cardiac output by the thermodilution method was performed in subjects without respiratory function disturbance during right heart catheterization. After the measurement of cardiac output, the subjects rebreathing a gas mixture containing acetylene and argon from the end tidal level. The inspiratory and expiratory gases were measured by a mass-spectrometer. Results were analyzed by a lung model consisting of two compartments (rebreathing bag compartment and lung compartment), while taking into account the volume reduction due to O2 and CO2 exchange and the fluctuation of end tidal gas concentration until equilibrium between the bag and the lung. The correlation coefficient between these two methods was 0.944, which was statistically significant. The regression line was near the line of identity. The measurement of pulmonary blood flow by the acetylene rebreathing method was applicable in cases without lung function disturbance.

Acetylene↗

Pentoxifylline does not attenuate acute lung injury in the absence of granulocytes.

Pentoxifylline (PTX), a methylxanthine, can suppress polymorphonuclear leukocyte (PMN) activation and attenuate sepsis-induced acute lung injury. We investigated whether PTX prevents non-PMN-dependent lung injury. First we studied four groups of granulocyte-depleted guinea pigs (control, PTX, Escherichia coli, and E. coli + PTX). Lung injury was assessed by wet-to-dry lung weight (W/D) ratio and lung tissue-to-plasma 125I-albumin ratio (albumin index, AI). The E. coli group showed a significant increase in the lung W/D ratio and AI compared with the control and PTX groups. However, PTX did not prevent the E. coli-induced increase in the lung W/D ratio and AI. Next we investigated the effects of PTX on endothelial cell monolayer permeability and adenosine 3',5'-cyclic monophosphate (cAMP) levels. Whereas E. coli lipopolysaccharide (LPS) alone increased the endothelial permeability, PMNs added to the endothelial monolayers and exposed to LPS enhanced the increase. PTX attenuated the permeability increase mediated by LPS-exposed PMNs. PTX did not prevent the LPS-induced increase in permeability when PMNs were not present, although PTX increased endothelial cell cAMP levels. These data demonstrate that 1) PTX does not prevent lung injury in granulocyte-depleted guinea pigs; 2) PTX does not prevent LPS-induced increases in endothelial cell permeability, despite increased cAMP levels; and 3) PTX attenuates PMN-dependent increases in endothelial cell permeability.

Animals↗

Early post-treatment with pentoxifylline or dibutyryl cAMP attenuates Escherichia coli-induced acute lung injury in guinea pigs.

We examined effects of early post-treatment with the methylxanthine pentoxifylline (PTXF), or the cell-permeable adenosine 3', 5'-cyclic monophosphate (cAMP) analog dibutyryl cAMP (db-cAMP) on Escherichia-coli-induced acute lung injury in guinea pigs. Acute lung injury was assessed by measurements of lung water (lung wet/dry weight ratio; W/D ratio), the concentration ratio of 125I-albumin in bronchoalveolar lavage (BAL) fluid and lung tissue compared with plasma (albumin index; BAL-AI or tissue-AI), and total differential leukocyte count in BAL fluid. Mean arterial pressure (Pa) and peripheral WBC counts were monitored continuously over the 8-h experiment. Septicemia was induced by a bolus injection of 2 x 10(9)/kg live E. coli. Thirty minutes later the animals received a bolus injection followed by continuous infusion of PTXF (20 mg/kg + 20 mg/kg/h; n = 8) or db-cAMP (2 mg/kg + 2 mg/kg/h; n = 8) or saline (septic control; n = 8). Nonseptic control groups were also studied. The lung W/D ratio, BAL-AI, lung tissue-AI, and BAL leukocyte count increased significantly in the septic control group. The PTXF-septic and db-cAMP-septic groups showed no significant increase in lung W/D ratio, BAL-AI, and lung tissue-AI. However, there was no difference in BAL total and differential leukocyte count as compared with the septic control group. PTXF and db-cAMP had no effect on E. coli-induced changes in peripheral WBC count and Pa. Comparison in vitro experiments demonstrated that PTXF and db-cAMP inhibited the endotoxin-induced (E. coli) chemiluminescent response of isolated guinea-pig polymorphonuclear leukocytes (PMN).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[A case of Legionnaires' disease cured with a combination of erythromycin and steroid therapy].

A 53-year-old male was admitted to Keio University Hospital with a pneumonia shadow in the left lung field and respiratory failure. Because there was progression of respiratory failure, mechanical ventilation was required to maintain appropriate oxygenation. Although erythromycin administration was started at the time of admission, a steroid (prednisolone 60 mg/day) was added a few days later to temporarily inhibit the acute inflammatory response in the lung parenchyma. This intensive therapy resulted in resolution of the patient's pneumonia and improvement of his respiratory failure. No pathogens were detected in the clinical specimens. Indirect immunofluorescence examination demonstrated a marked increase in titers against Legionella pneumophila serogroup 1, which was sufficient to confirm a diagnosis of Legionnaires' disease. The causative organism of this disease, a gram-negative short rod, is rarely cultured on conventional culture media. Two clinical subtypes are known based on clinical manifestations: 1) the Pontiac fever-type in which the predominant symptom is fever alone; and 2) the pneumonia-type which was observed in the epidemic in Philadelphia when the disease was first reported in 1976. The present case of Legionnaires' disease was the severe pneumonia-type which was successfully treated with a combination of erythromycin and a steroid.

Drug Therapy, Combination↗

[Changes in sound transmissibility through the canine thorax due to the experimental pleural effusion].

The authors studied the effects of pleural effusion on sound transmissibility through the canine thorax. In the supine position, dogs received sound ranging from 100 to 1000 Hz at the tracheostoma. Using the microphones attached to the dorsal and ventral part of the chest wall, the relative level of the transmitted sound wave was determined in reference to the amplitude of the sound wave at a tracheostom. Measurements of sound transmissibility were performed before and after injecting saline into the bilateral pleural space which was intended to be experimental pleural effusion. In the dorsal part, the experimental pleural effusion decreased sound transmissibility in the frequency range between 100 and 300 Hz. At 100 Hz, the pleural effusion of 5, 10, and 15 ml/kg/hemithorax caused a decrease in sound transmissibility by 3.7 +/- 3.7, 6.6 +/- 4.9, and 10.0 +/- 5.7 dB, respectively. In the ventral part, the reduction in sound transmissibility in the low frequency range due to the pleural effusion was small. In contrast, introduction of pleural effusion caused an increase in sound transmissibility by 5 to 9 dB in the frequency range above 500 Hz. We consider that these changes in sound transmission are implicated in the physical findings such as "aegophony" and reduction in vocal fremitus or vocal ausculation.

Animals↗

Prevention of interleukin 2-induced acute lung injury in guinea pigs by pentoxifylline.

We administered recombinant human interleukin 2 (IL-2) to guinea pigs to investigate whether IL-2 would cause acute lung injury. In addition, we examined the effects of pentoxifylline (PTXF) on IL-2-induced acute lung injury. Three groups of animals were studied over a period of 8 h. The saline control group was injected intravenously with 2 ml of pyrogen-free saline; the IL-2 group was injected intravenously with 4 X 10(6) U/kg recombinant IL-2; and the IL-2-PTXF group was injected with a 20-mg/kg bolus of PTXF followed by a continuous infusion (6 mg.kg-1.h-1) started 60 min before injection of 4 X 10(6) U/kg IL-2. Lung water (wet-to-dry lung weight ratio), the concentration ratios of 125I-albumin in bronchoalveolar lavage (BAL) fluid and lung tissue compared with plasma (125I-albumin BAL-to-plasma, 125I-albumin lung-to-plasma), and cell counts in BAL fluid were examined. An intravenous injection of IL-2 caused an increased lung water (P less than 0.01), an increased 125I-albumin lung-to-plasma ratio (P less than 0.05), and a significant increase in the absolute number of neutrophils, lymphocytes, and macrophages in BAL fluid compared with the saline control. In contrast, the PTXF-pretreated group did not demonstrate IL-2-induced acute lung injury (lung water, 125I-albumin lung-to-plasma) or increased accumulation of neutrophils, lymphocytes, and macrophages in the BAL. These data suggest a possible role for PTXF in attenuating the side effects of IL-2.

Acute Disease↗

Pentoxifylline prevents tumor necrosis factor-induced lung injury.

Human tumor necrosis factor-alpha (TNF) is a monokine produced by mononuclear cells after many stimuli, including bacterial endotoxin. Full exploration of its antineoplastic effects has been limited by side effects. We have previously shown that the administration of TNF to guinea pigs is associated with a syndrome similar to gram-negative septic shock, which includes capillary permeability lung injury. In this study, we measured the effects of pentoxifylline (PTX) on parameters of TNF-induced lung injury including: lung wet-to-dry weight ratio, the ratio of lung-to-plasma 125I-labeled albumin (albumin index), bronchoalveolar lavage (BAL) and peripheral leukocyte counts, and serial measurements of mean arterial pressure (MAP). Four groups of animals were studied: a TNF group received 3.75 x 10(6) U/kg TNF; a PTX group received a 20-mg/kg bolus of PTX followed by an infusion of 6 mg/kg/h; the PTX-TNF group received both; and the final group was a saline control. ANOVA analysis revealed significant elevations of lung wet-to-dry ratio only in the TNF group (5.9 [5.6 to 6.3], p less than 0.001), expressed as the mean followed by 95% confidence intervals). Lung albumin index was elevated only in the TNF group (0.24 [0.19 to 0.29], p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The effects of aminophylline and pentoxifylline on multiple organ damage after Escherichia coli sepsis.

We studied the effects of the methylxanthines, aminophylline (AMPH) and pentoxifylline (PTXF), on multiple organ damage following Escherichia coli sepsis in guinea pigs. To assess multiple organ damage, 125I-labeled albumin accumulation was measured in bronchoalveolar lavage (BAL) fluid, lung, kidneys, liver, heart, adrenal glands, and spleen and expressed as a ratio of BAL fluid or tissue to 125I-labeled albumin plasma (albumin index: Al). Wet-to-dry lung weight (W/D) ratios were also measured. The methylxanthines were administered by a bolus injection followed by a continuous infusion. The seven experimental groups included: saline-control, AMPH-control, PTXF-control, E. coli septic-control, E. coli septic-AMPH high dose, E coli septic-AMPH low dose, and E. coli septic-PTXF. The AI of the BAL fluid and all examined organs significantly increased in the septic-control group compared to those in the saline-, AMPH-, and PTXF-control groups, In all septic-methylxanthine groups, the AI of the BAL fluid and all organs, except for the spleen, were significantly lower than those of the septic-control group. Compared to the saline-, AMPH-, and PTXF-control groups, the septic-control group revealed a significant increase in lung W/D ratios, whereas the septic-AMPH high and low dose groups and the septic-PTXF group did not. Of importance, the septic-PTXF group did not cause a significant decrease in mean arterial pressure (MAP) as compared to the control groups, whereas the septic-AMPH groups did cause a significant decrease in MAP compared to the septic-control group. Therefore, the data from this experiment demonstrate that both AMPH and PTXF attenuate the multiple organ albumin leak seen in septic guinea pigs. However, PTXF exerted this protective effect with no discernible effect on the MAP whereas the MAP of AMPH-treated guinea pigs was significantly decreased.

Albumins↗

Effects of tumor necrosis factor on PMN chemotaxis, chemiluminescence, and elastase activity.

Tumor necrosis factor (TNF) has been proposed as an important mediator of the inflammatory response in acute lung injury. To better understand polymorphonuclear leukocyte (PMN) activation during acute lung injury, we evaluated the effects of TNF on several in vitro PMN functions, including chemotaxis, chemiluminescence, and elastase activity. In the chemotaxis assay using a modified Boyden chamber, TNF alone or with N-formyl-methionyl-leucyl-phenylalanine (FMLP, 10(-8) mol/L) did not alter PMN migration. TNF suspended with 1% zymosan-activated serum (ZAS) increased PMN migration at low concentrations and decreased migration at high concentrations (control 99 +/- 4.8 microns, n = 9; TNF 0.1 ng/ml 135 +/- 9.4 microns, n = 5, p less than 0.01; TNF 1000 ng/ml 62 +/- 7.5 microns, n = 5, p less than 0.01). In the chemiluminescence assay, TNF (1000 ng/ml) induced a 3-fold increase in the PMN chemiluminescent response. However, TNF incubated with PMN did not cause an increase in supernatant elastase activity. These data reveal TNF induced the production of PMN reactive oxygen species as evidenced by an increased chemiluminescent response. Whereas TNF increased chemotaxis at low concentrations in the presence of 1% ZAS, high concentrations of TNF similar to levels detected in septic shock caused a decrease in chemotaxis that might contribute to retaining PMN in sites of inflammation. It is thus suggested that TNF may contribute to inflammation by stimulating the production of PMN-reactive oxygen species and modulating-PMN chemotaxis.

Acridines↗