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T Tanita

Publications and source records attributed to T Tanita.

At least 19 recordsLinked to original sources
PubMed1998

Prognostic assessment of 1310 patients with non-small-cell lung cancer who underwent complete resection from 1980 to 1993.

OBJECTIVE: The TNM staging system of lung cancer is widely used as a guide for estimating prognosis and selecting treatment modality. In 1997, the International Union Against Cancer and the American Joint Committee on Cancer have adopted a revised stage grouping for lung cancer. However, the validity of the new stage grouping has not been fully established. We investigated the prognoses of patients who had resection of non-small-cell lung cancer to confirm the validity of the revised classification. METHODS: A total of 1310 patients with non-small-cell lung cancer underwent complete resection and pathologic staging of the disease in our hospitals from 1980 through 1993. A pulmonary resection was performed with a systematic nodal dissection. The survivals were calculated with the Kaplan-Meier method on the basis of overall deaths, and the survival curves were compared by log rank test. RESULTS: There were significant differences in survival between patients with T1 N0 M0 and T2 N0 M0 disease and between those with T1 N1 M0 and T2 N1 M0 disease. However, there was no significant difference between patients with T2 NO M0 disease and those with T1 N1 M0 disease. No significant difference in survival was observed among patients with T2 N1 M0, T3 NO M0, and T3 N1 M0 cancer. Patients with different invaded organs of T3 subdivision (pleura, chest wall, pericardium, or diaphragm) had a different prognosis. There was no significant difference between patients with T3 N2 M0 disease and those with stage IIIB disease. CONCLUSIONS: We supported most of the revision, such as dividing stage I, dividing stage II, and putting T3 N0 M0 to stage IIB. Furthermore, we found some candidates for a subsequent revision, such as putting T3 N1 M0 to stage IIB, putting T2 N0 M0 and T1 N1 M0 together, regarding diaphragm invasion as T4, and putting T3 N2 M0 to stage IIIB.

Carcinoma, Non-Small-Cell Lung↗
PubMed1998

[Preoperative endovascular ultrasonography in lung cancer patient for detecting aortic wall invasion: a case report].

A 69-year-old man was admitted to our hospital because of left primary lung cancer. As tumor invasion to the descending artery was suspected, preoperative endovascular ultrasonography was performed. Part of the wall lacked respiratory movement. However, the wall of the descending artery was visualized as three layers, i.e., hyper-, hypo- and hyperechoic layers by sonography, so tumor invasion to the descending artery was diagnosed as negative. Although inflammatory tumor adhesion to the descending artery was found, left upper lobectomy was safely performed. Endovascular ultrasonography was considered to be useful in marking an accurate diagnosis of tumor invasion to the descending artery.

Aged↗
PubMed1998

[Increase in pulmonary vascular permeability caused by increased adhesiveness of polymorphonuclear leukocytes and superoxide].

We report that mechanical stimulation of human neutrophils results in their accumulation in isolated rat lungs and in an increase in pulmonary vascular permeability. To determine whether reactive oxygen species were involved in this increase and, if so, whether it is mediate by xanthine oxidase metabolites, we assessed the effect of stimulated and unstimulated neutrophils, and of a superoxide scavenger, superoxide dismutase (SOD), and a xanthine oxidase inhibitor, allopurinol (ALLO) on pulmonary vascular permeability in isolated perfused lungs from Sprague-Dawley rats. Pulmonary vascular permeability in isolated rat lungs was assessed using a filtration coefficient determined by gravimetry. To quantify neutrophil accumulation in the lung, we measured myeloperoxydase (MPO). Neutrophils were stimulated by gentle agitation in a glass container for 10 s and Mac-1 was subsequently upregulated on the surface of the neutrophils. In lungs that received stimulated neutrophils, the pulmonary vascular filtration coefficient was about 5 times higher than in lungs that received unstimulated neutrophils. An increase in filtration coefficient was almost completely blocked by pretreatment with SOD or ALLO. However, the accumulation of stimulated neutrophils was not, or only partly, blocked by SOD or ALLO, respectively. We conclude that the increase in pulmonary vascular permeability caused by mechanically stimulated neutrophils was partly mediated by reactive oxygen species generated via the xanthine oxidase system.

Animals↗
PubMed1998

[Prognosis of T3 patients with resected non-small cell lung cancer according to the invaded organs].

We investigated the prognosis of completely resected 119 non-small cell lung cancer patients according to the invaded organs. There was no significant difference in prognosis between T3N0M0 and T3N1M0 patients (5-year survival rate: 34% vs. 38%). However, the prognosis of T3N2M0 patients (5-year survival rate: 11%) was too poor to be regarded as the same category. Therefore, we investigated only T3N0M0 and T3N1M0 patients to assess the contribution of the invaded organs to prognosis. Of the 5 patients with diaphragm invasion, there was no 3-year survivor, and the prognosis of patients with diaphragm invasion was very poor. The chest wall invasion was divided into three parts: parietal pleural invasion, subpleural tissue invasion and intercostal muscular invasion. The 5-year survival rates of patients with such invasion was 35%, 29% and 27%, respectively. The patients with Pancoast tumor had very poor prognosis. T3 factor was heterogeneous, and the prognosis of the patients with T3 tumor was various according to invaded organs.

Adult↗
PubMed1998

Chromosome bands 3p14.2, 9p21, and 13q14 are frequently deleted in roentgenographically occult bronchogenic squamous cell carcinoma of the lung.

Roentgenographically occult bronchogenic squamous cell carcinomas are early lung cancers that localize mainly within the bronchial wall and are thought to be a good model for elucidating chromosomal alterations during lung cancer progression. In this study, we analyzed allelic losses on chromosome regions 1p36, 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, in which there are putative tumor suppressor genes that may play roles in lung carcinogenesis. Forty-five cases with roentgenographically occult bronchogenic squamous cell carcinoma (ROC) and 47 cases of bronchogenic carcinoma with abnormal shadows (roentgenographically nonoccult bronchogenic squamous cell carcinoma [RNOC]) were examined. Highly frequent LOHs in both ROCs and RNOCs were observed in chromosome regions 3p14.2, 9p21, and 13q14.1-q14.2. LOHs were more frequently observed in RNOCs than in ROCs at two loci: 10q25.3-q26.1 and 16q24.1-q24.2. These results suggested that (1) putative tumor suppressor genes exist on 3p14.2, 9p21, 10q25.3-q26.1, 13q14.12-q14.2, and 16q24.1-q24.2, which may play important roles in lung carcinogenesis; (2) mutations in genes at 3p14.2, 9p21, and 13q14.12-q14.2 represent rather early events in lung carcinogenesis; and (3) mutations in genes on 10q25.3-q26.1 and 16q24.1-q24.2 represent rather late events.

Aged↗
PubMed1997

Vasoactive intestinal peptide causes nitric oxide-dependent pulmonary vasodilation in isolated rat lung.

Vasoactive intestinal peptide (VIP) is one of the chief neurotransmitters of nonadrenergic noncholinergic nerve fibers. In this study, we investigated the effect of VIP on the pulmonary circulation in isolated perfused rat lungs. Baseline pressures of the pulmonary artery for the isolated rat lungs were not affected by 3 x 10(-8) M VIP. VIP caused dose-dependent pulmonary vasodilation when the pulmonary vascular bed was constricted with 20 mM KCl. This vasodilative effect of VIP was inhibited by 1 x 10(-6) M L-n omega-nitro-arginine, an endothelium-derived relaxing factor (nitric oxide) inhibitor, and was restored by the addition of 10(-4) M L-arginine, a substrate of nitric oxide. VIP also caused suppression of the ANG II pressor response, and this VIP-induced suppressive effect was reduced when L-N omega-nitro-arginine or 3 x 10(-6) M meclofenamate was added to the perfusate. These results indicate that VIP causes pulmonary vasodilation in isolated rat lung and suggest the possible involvement of NO and/or cyclooxygenase metabolites in VIP-induced pulmonary vasodilation.

Angiotensin II↗
PubMed1997

Roles of the visceral pleura in the production of pleural effusion in permeability pulmonary edema.

We investigated the roles of the mesothelium of the visceral pleura on hydraulic conductivity in dogs under normal conditions and condition of permeability pulmonary edema. Nineteen mongrel dogs were divided into following 4 groups: thoracotomy alone (control group, n = 7); thoracotomy and striping of the mesothelium using Gelfilm (C + G group, n = 4); injection of oleic acid to increase the permeability of the pulmonary vessels (OA group, n = 4); injection of oleic acid and striping of the mesothelium (OA + G group, n = 4). A hemispherical capsule filled with physiological saline was attached to the visceral pleura. The transpleural fluid flow (delta V) was measured at given incremental or decremental hydrostatic pressures (delta Pcap) in the capsule. Hydraulic conductivity was calculated from the slope of linear regression line obtained from relationship between delta Pcap and the fluid flow rate (v) according to the Starling's equation. The conductivity obtained were 1.49 +/- 0.69 (nl.min-1.cmH2O-1.cm-2) in the control group, 1.37 +/- 0.88 in the C + G group, 3.75 +/- 0.74 in the OA + G group, and 7.07 +/- 2.49 in the OA + G group. The hydraulic conductivity was not increased by striping of the mesothelium (1.49 +/- 0.69 [nl.min-1.cmH2O-1.cm-2] vs. 1.37 +/- 0.88, in the control group vs. C + G group, respectively). Visceral pleural hydraulic conductivity following OA injection was increased by striping of the mesothelium (3.75 +/- 0.74 vs. 7.07 +/- 2.49 in OA group vs. OA + G group, respectively). These findings suggest that the wall of pulmonary vessels acts as a barrier to movement of pleural effusion under normal conditions, whereas the mesothelium of the visceral pleura acts as that under condition of permeability pulmonary edema.

Animals↗
PubMed1997

Cyclooxygenase metabolites possibly produced by endothelial cells mediate the lung injury caused by mechanically stimulated leukocytes.

To determine whether mechanically stimulated leukocytes increase pulmonary vascular permeability and resistance and, if so, whether cyclooxygenase metabolites mediate the increase, we assessed the effects of stimulated and unstimulated leukocytes, and of a cyclooxygenase inhibitor on pulmonary vascular permeability and resistance in isolated perfused lungs from Sprague-Dawley rats. Leukocytes were stimulated by gentle agitation in a glass container for 10 seconds. After baseline measurements were made, stimulated or unstimulated leukocytes were added to the perfusate. The effects of the cyclooxygenase inhibitor, meclofenamate, on the pulmonary vascular filtration coefficient and pulmonary vascular resistance were measured. In the rats that received stimulated leukocytes, the pulmonary vascular filtration coefficient and the vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the rats that received unstimulated leukocytes. These increases were completely and partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of leukocytes to the pulmonary vascular endothelium. These findings suggest that mechanically stimulated leukocytes increase pulmonary vascular permeability and that cyclooxygenase metabolites produced by endothelial cells may injure the cells.

Animals↗
PubMed1997

[A case of systemic origin of an aberrant artery to the basal segment of the lung].

We report on a rare case of systemic origin of an aberrant artery to the basal segment of the lung (Pryce I type intralobar pulmonary sequestration) that caused occasional bloody sputum. The patient was admitted to our hospital after an abnormal image was discovered in Chest X-ray film. The chest MRI showed an abnormal vessel originating from the descending aorta. The aortagram showed an abnormal artery originating from the descending aorta and entering the left lower lobe, and the left pulmonary angiogram revealed a poorly blood supply to the left basal segments. The preoperative diagnosis of systemic origin of an aberrant artery to the basal segment of the lung was given. The patient was subjected to surgical treatment. During surgery, it was found that the abnormal artery, 12 mm in diameter, which was connected from the descending aorta to the left basal segments. The abnormal artery was dissected, and the left basal segments was removed. The postoperative course was uneventful.

Aorta, Thoracic↗
PubMed1997

[Role of leukotriene B4 in monocrotaline-induced pulmonary hypertension].

Monocrotaline (MCT) causes lung inflammation and chronic pulmonary hypertension associated with lung vascular thickening in rats. We hypothesized that leukotriene B4 (LTB4) and LTB4-induced accumulation of leukocytes in the lung play a role in MCT-induced lung disease, and therefore measured LTB4 and myeloperoxidase (MPO) levels in lung tissue of MCT-treated rats. Next, we examined the effect of an orally active LTB4 receptor antagonist (ONO4057) on MPO levels in lung tissue, on pulmonary hypertension, and on pulmonary vascular remodeling induced by MCT. Lung LTB4 and MPO levels had increased by 3 days after MCT injection. In the ONO4057-treated MCT rats, lung MPO levels were significantly lower than in the rats given MCT but not ONO4057. By the third week after injection. MCT had caused increases in mean pulmonary arterial pressure, in the ratio of right ventricular weight to left ventricle+septum weight (RV/[VS + S]), and in media wall thickness of the muscular arteries of the lung. Treatment with ONO4057, either for 3 weeks or during the first week after MCT injection, significantly reduced pulmonary hypertension, right ventricular hypertrophy, and lung vascular thickening induced by MCT. These results indicate that ONO4057 reduces both the accumulation of leukocytes in lung tissue and the chronic pulmonary hypertension induced by MCT, and they suggest a role for LTB4 in the inflammatory process that contributes to pulmonary hypertension and lung vascular remodeling induced by MCT in rats.

Animals↗
PubMed1997

[Early postirradiation changes in Na+ and fluid transport across alveolar epithelium in rats].

To study changes in Na+ and fluid transport that occur soon after irradiation of the thorax, we used fluid-filled isolated rat lungs. Irradiation 15 Gy of 60Co doubled the fluid absorption rate across the alveolar epithelium within 2 weeks, but fluid absorption had returned to the baseline values by 3 weeks after irradiation. The timing of this change in fluid absorption was parallel to the time course of Na+ escape across alveolar epithelium and the two correlated closely. These data suggest that a dysfunction of alveolar epithelial Na+ transport is involved in the development of pulmonary edema after irradiation of the thorax.

Animals↗
PubMed1997

[Effect of thoracoscopic procedure versus standard posterolateral/muscle-sparing thoracotomy on pulmonary lung function].

To understand the effects of thoracoscopic approach to thoracotomy on lung function, we investigated the changes in lung function after thoracoscopic operation (n = 7) and compared them to those after standard posterolateral (n = 5) or muscle-sparing thoracotomy (n = 6). In 18 patients with benign lung tumor in which surgical treatment resected in partial resection of the lung tissue, we measured TLC, VC, RV, FEV1.0, FEV1.0%, Peak Flow and DLco preoperatively and at 2, 4 weeks postoperatively. In the standard posterolateral or muscle-sparing thoracotomy groups, FVC, TLC, FEV1.0 and Peak Flow decreased to about 80% of preoperative value at 2 weeks. At 4 weeks after operation, these values showed to increase some what, but did not reach to the preoperative value. Whereas, the thoracoscopic procedure group, did not show the decrease in lung function through the time course. There was not significant different between standard posterolateral and muscle-sparing thoracotomy. We conclude that thoracoscopic approach is an useful technique to thoracotomy because of its minimizing after thoracotomy effect of lung function loss.

Adult↗
PubMed1997

[Increase in pulmonary vascular permeability caused by increased expression of Mac-1 on the surface of polymorphonuclear leukocytes].

We studied the expression of adhesion molecules on the surface of human polymorphonuclear leukocytes (PMNs). The effects of mechanical stimulation were measured with a flow cytometer and pulmonary vascular injury due to accumulation of PMNs in the lungs was assessed by a gravimetric method. The accumulation of PMNs in the lungs was studied by measuring the amount of myeloperoxidase. PMNs were stimulated by gentle agitation in a glass container for 10 s. Mac-1 (CD11b/CD18) was upregulated on the surface of PMNs that were mechanically stimulated. When unstimulated PMNs were exposed to isolated rat lungs, the filtration coefficient did not change from that under baseline conditions. However, when mechanically stimulated PMNs were exposed to isolated rat lungs, the filtration coefficient was about 5 times higher than that measured at baseline. When mechanically stimulated PMNs treated with anti-CD18 antibody were used, the increase in the filtration coefficient was completely blocked. The assay of myeloperoxidase revealed that PMNs stuck to isolated rat lungs only after stimulated PMNs were added. We conclude that when the adhesiveness of PMNs is increased by mechanical stimulation, these cells adhere to pulmonary vessels and increase pulmonary vascular permeability.

Animals↗
PubMed1997

[Prediction of postoperative pulmonary hemodynamics for the second lobectomy after the contralateral lobectomy].

We presented 7 cases who were performed the second lobectomy for the second lung cancer after the first successful lobectomy on the contralateral lung (3 cases for right upper lobectomy + left lower lobectomy and 4 cases for right upper lobectomy + left lower lobectomy). In 6 patients, the predicted postoperative FEV1 estimated by multiplying the preoperative FEV1 by the fraction of perfusion to the contralateral lung was less than 800 ml/m2BSA, which is our first cut-off for identifying lung resection candidates. Unilateral pulmonary arterial occlusion test (UPAO) revealed that total pulmonary vascular resistance (TPVRI) in 3 of those 6 patients was lower than 700 dyne.sec.cm-5/m2BSA, our second cut-off for lung resection. More precise postlobectomy pulmonary hemodynamics in another 3 of those 6 patients were then estimated by adapting selective pulmonary occlusion test (SPAO). Since TPVRI during SPAO was lower than the cut-off value, it was suggested that second lobectomy would be feasible with low incidence of post operative cardiopulmonary complication. There was no serious complications in all 7 cases during their postoperative course. We believe that more precise prediction of postoperative pulmonary hemodynamics by adapting UPAO and SPAO could be one of the tools to minimumize postoperative cardiopulmonary complications in those patients needed second lobectomy for the second lung cancer after the first successful lobectomy on the contralateral lung even though their impaired lung fung function.

Aged↗
PubMed1997

[Video-assisted thoracoscopic surgery of bilateral dissemination of invasive thymoma: report of a case].

Eight years ago, A 29-year-old woman was admitted by complaining with facial edema and dyspnea. A chest x-ray film and computed tomography showed an anterior mediastinal tumor that invaded to the superior vena cava and the trachea. A bronchoscopic biopsy revealed that the tumor was a thymoma. We performed radiotherapy and chemotherapy because a surgical operation was not possible. The size of the tumor was slightly reduced after those therapies roentgenographically. We followed up the subsequent of history of the patient. Eight years later, July, 1995, chest computed tomography showed bilateral disseminations of invasive thymoma. The disseminated tumors were removed by two-stage video assisted thoracoscopic surgery (VATS), to preserve collateral veins so that collateral venous circulations were preserved. She discharged 20 days after second VATS uneventfully.

Adult↗
PubMed1997

[Thoracic surgery and liver dysfunction].

Lung resection results in loss of lung parenchyma including residual healthy lung tissue and in reduction in pulmonary vascular bed. A decrease in residual pulmonary vascular bed after lung resection causes an increase in right heart afterload, and in some patients, it would be associated with an increase in right heart preload and consequent the changes in hepatic circulation which would lead to liver damage. Preceding thoracotomy, unilateral pulmonary arterial occlusion test (UPAO) was performed to simulate the hemodynamic changes after lung resection to evaluate the increase in right heart preload after surgery. Patients with the decreases in cardiac index or PaO2 during UPAO showed a higher levels of GPT during postoperative period when compared with those with the increase in either parameters. In a surgical treatment for empyema, bronchiectasis, or other infectious lung diseases, bronchial angiography (BAG) and also bronchial arterial embolization (BAE) were useful methods to prevent from exceeding bleeding during thoracotomy, which is one of the risk factors to cause liver damage after surgery. These results suggest that, in the field of thoracic surgery, the preoperative assessment of the hemodynamic changes caused by lung resection and the preoperative attempt to prevent from bleeding during thoracotomy are both important to protect from liver damage caused by surgical stress.

Empyema↗
PubMed1997

[A case of lung abscess with elevated serum levers of sialyl Lewis X-i (SLX) and CA 19-9].

A case of lung abscess of the felt lower lobe in a 19-year-old woman with elevated serum levels of Sialyl Lewis X-i (SLX) and CA 19-9 is reported. Completing the lobectomy, serum SLX level returned to the normal range within a week postoperative day. Serum CA 19-9 level also decreased at half life of 2 weeks to the normal range within 6 weeks postoperative day. Laboratory examination demonstrated high levels of these antigens in abscess fluid. Histologically, the abscess was revealed to be associated with a markedly dilated bronchus with hyperplastic bronchial glands, and there was no evidence of malignancy. Immunohistochemical examinations using monoclonal antibodies against human SLX and CA 19-9 showed highly positive reaction with those antigens in both goblet cells in bronchial epithelia and the mucous cells in bronchial glands.

Adult↗