Search PubMed⌕ Search

Biomedical subjects

M Oda

Publications and source records attributed to M Oda.

At least 145 records · Page 8Linked to original sources

[Evaluation of new TNM classification for lung cancer, especially T3N0M0, stage IIIA, stage IIIB, and pm].

The purpose of this study was to evaluate the results of new TNM staging system for lung cancer in 1997, especially T3N0M0, stage IIIA, stage IIIB, and pm. Five-year survival rates of the patients with stage IIIA and stage IIIB were 16% and 18% respectively (NS). Five-year survival rates of patients with T3N1M0, T1N2M0, T2N2M0, and T3N2M0 were 40%, 28%, 15%, and 3%, respectively. The prognosis of T3N2M0 was significantly worse than that of T3N1M0, T1N2M0, and T2N2M0. Five-year survival rates of the patients excluding pm 1 with T4N0M0, T4N1M0, T4N2M0, and T4N3M0 were 21%, 10%, 10%, and 0%, respectively. The prognosis of the patients with T4N0 was significantly better than that of T4N2 and T4N3. In the patients with pm, 5-year survival rates of the patients with pm 1 and pm 2 were 26% and 7%, respectively (p < 0.01). In the patients with pm 1, 5-year survival rates of the patients with N0 + N1 and N1 + N2 were 53% and 16%, respectively (p < 0.01). From our these results, we supported the new TNM system as putting T3N0M0 to stage IIB, putting pm 2 into stage IV. We proposed; 1) chest wall invasion with bone destruction stay in stage IIIA or is T4, 2) T3N1M0 is classified with stage IIB, 3) main stem bronchus invasion is classified with T2, 4) pm 1 is subdivide by N status. Furthermore, stage III seemed to be reasonably subdivided into T1-2N3M0, T4N0-1M0 as stage IIIA and T3-4N2, T1-4N3 as stage IIIB.

Humans↗

[A case of panpleuropneumonectomy for diffuse pleural mesothelioma].

A 58-year-old man was admitted to our hospital because of chest pain and dyspnea on July 15, 1999. A chest X-ray showed left pleural effusion, and a chest CT revealed left pleural effusion and diffuse pleural thickening. Because pleural fluid cytology and percutaneous needle pleural biopsy were negative for malignancy, thoracoscopic biopsy was performed on July 28. The biopsied specimen revealed malignant pleural mesothelioma (epithelial type). An operation was performed on August 16. First, mediastinal lymph node dissection was performed and we identified that there was no lymph node metastasis by frozen section diagnosis. Then panpleuropneumonectomy with combined resection of the diaphragm and pericardium was performed.

Diaphragm↗

Intrapulmonary lymph nodes detected by exploratory video-assisted thoracoscopic surgery: appearance of helical computed tomography.

The objective of this study was to analyze helical computed tomography (CT) findings of intrapulmonary lymph nodes (IPLNs), and to evaluate the diagnostic procedures to prevent unnecessary exploratory surgery. Between April 1997 and March 2000, we performed exploratory video-assisted thoracoscopic surgery (E-VATS) in 42 patients and in 8 patients (4 men, 4 women; 48 to 75 years of age, mean 57 years) IPLN was pathologically proven. Retrospectively, the appearances of IPLN in helical CT images were studied in detail. The diameter of the IPLNs varied from 4 to 10mm. Six nodules were located in the lower lobes and 2 nodule was in the lingula. Chest CT showed several malignancy-suggesting associated findings with pleural indentation (2/8), spicular radiation (2/8), fuzzy margins (4/8), and vascular involvement (2/8). Black colored anthracoses in 5 subpleural IPLNs were confirmed by thoracoscopy. One patient with two coin lesions was suggestive of lung metastasis of adenoidcystic carcinoma of the tongue, but one lesion was proven as IPLN, and the other as metastatic carcinoma. In conclusion, it is not possible to distinguish an intrapulmonary lymph node from a malignant lesion using the CT findings preoperatively. Therefore, a pathological study with E-VATS is necessary and sure procedure to exclude malignant disease under the present conditions.

Aged↗

[A case of acute motor sensory axonal polyneuropathy after Haemophilus influenzae infection].

A 47-year-old woman developed consciousness disturbance, and experienced hallucinations while traveling abroad, and then went into critical condition. She was placed in the critical care unit, and had flaccid tetraparesis requiring mechanical ventilation. Haemophilus influenzae was cultured from the sputum. The level of protein of the cerebrospinal fluid was elevated to 114 mg/dl, nerve conduction study showed findings of pure axonal damage, and the sural nerve biopsy revealed severe axonal degeneration. She improved gradually by plasma exchange. The diagnosis of acute motor sensory axonal polyneuropathy (AMSAN) based on autoimmune mechanism was made. We speculate that H. influenzae infection may have elicited AMSAN in this case.

Autoimmunity↗

Endothelial cell dysfunction in microvasculature: relevance to disease processes.

Functional and morphological alterations of microvascular endothelial cells (ECs) would lead to microcirculatory disturbances, thereby providing a basis for the development of a disease state. Clinically endotoxemia frequently encountered in a variety of diseases is considered to be a trigger to develop the microcirculatory disorders such as disseminated intravascular coagulation (DIC) and multiple organ failure (MOF), both of which feature the end stage of severe systemic disease. Experimentally intravital microscopy reveals that continuous venous infusion of endotoxin (LPS) causes a low flow state in the rat mesenteric microcirculatory unit. By vital stain with monastral blue B (MBB), the microvascular ECs are focally positive for MBB at the postcapillary venular site, where leukocytes adhere and extravasate. As shown in the histamine-induced diapedesis by transmission electron microscopy, the MBB-positve venular ECs may correspond to the contracted ECs, enabling the polymorphonuclear leukocytes and erythrocytes to extravasate through the widened gaps between the contracted ECs. Actin filaments proven in the microvascular ECs by electron microscopy may play a modulating role in this neutrophil diapedesis. In the process of gastric ulcer formation under restrained stress to the rat, the ECs of microvessels in the gastric mucosa, particularly of the mucosal capillaries and postcapillary venules directly innervated by the cholinergic nerves, are altered by the stress-induced overstimulation of the autonomic nerves, inducing the diapedesis of leukocytes and erythrocytes followed by hemorrhagic and ischemic injuries in the gastric mucosa. Liver cirrhosis also accompanies endotoxemia. The most prominent electron microscopic alterations of hepatic microvasculature are a decrease of hepatic sinusoidal endothelial fenestrae (SEF) both in diameter and in number, and the formation of basement membranes beneath the hepatic sinusoidal ECs. These ultrastructural changes would be induced by a most potent vasoconstrictor endothelin (ET)-1 through the overexpressed ET(A) and ET(B) receptors on the hepatic stellate cells and the sinusoidal ECs, contributing to the development of portal hypertension as well as to the disturbance in excretion of endotoxin into the bile canaliculi via the hepatocytes from the circulating sinusoidal blood to prevent endotoxemia.

Actin Cytoskeleton↗

Local regulators of hepatic sinusoidal microcirculation: recent advances.

This article reviews our recent studies on the local regulation of hepatic microcirculation with special reference to the inlet sphincter-like structures, the roles of sinusoidal endothelial cells and the mechanism of dynamic changes in the sinusoidal endothelial fenestrae (SEF) as well as in the terminal portal venules and the terminal hepatic arterioles induced by the potent vasoconstrictor endothelin (ET)-1. There are two types of sphincter-like structures at the entering sites of hepatic sinusoids. One is located at the junction between the terminal portal venule and the sinusoid, and is characterized by the large endothelial cells surrounded with Ito cells (hepatic stellate cells: HSCs). The other is located at the junction between the terminal hepatic arteriole and the sinusoid, and corresponds to the precapillary sphincter since our enzymohistochemical demonstration of arterial capillaries in close association with the sinusoids combined with intravital microscopy has revealed that the terminal hepatic arteriole directly terminates in the sinusoid. It is essential for the local control of hepatic sinusoidal blood flow that the dynamic contracting and relaxing changes not only in these inlet sphincter-like structures but also in the SEF correspond with those of the HSCs, both of which are mediated by the sinusoidal endothelium-derived vasoconstrictor endothelins (ETs) and vasodilator nitric oxide (NO). The contractility of the SEF and HSCs depends on the intracellular Ca++-calmodulin-actomyosin system.

Actomyosin↗

Multifocal polyradiculoneuropathy and carcinoma of the thymus.

We studied a patient with polyradiculoneuropathy with anaplastic carcinoma of the thymus. Motor manifestations dominated. Postmortem examinations indicated that the primary changes were in the spinal nerve roots, peripheral nerves and, possibly, the spinal anterior horn cells. The posterior funiculi and posterior root ganglia were also affected, implying multifocal and multiphasic degeneration. This unusual polyradiculoneuropathy is a form of carcinomatous neuropathy.

Aged↗

Construction of an artificial tandem protein of the c-Myb DNA-binding domain and analysis of its DNA binding specificity.

An artificial tandem protein was generated using the third repeat of the c-Myb DNA-binding domain, and its DNA binding affinity and specificity were analyzed by a filter binding assay, isothermal titration calorimetry, and surface plasmon resonance. Although this artificial protein had the proper secondary structure, which is similar to the third repeat by itself, it could not bind to the expected base sequences specifically. Compared with the successful results of the zinc finger fusion proteins with novel sequence specificities, the cooperativity between the adjacent repeats, observed in the c-Myb-DNA complex, should also be required for the DNA recognition by the artificial tandem protein. Using the previous analyses of the DNA binding specificities by Myb homologous proteins, the differences in the DNA recognition mechanisms between the animal and plant Myb domains are also discussed.

Amino Acid Sequence↗

Kinetic analysis of DNA binding by the c-Myb DNA-binding domain using surface plasmon resonance.

Kinetics of the interaction of the c-Myb DNA-binding domain (R2R3) with its target DNA have been analyzed by surface plasmon resonance measurements. The association and dissociation rate constants between the standard R2R3, the Cys130 mutant substituted with Ile, and the cognate DNA are 2.3x10(5) M(-1) s(-1) and 2.6x10(-3) s(-1) at pH 7.5 and 20 degrees C, respectively. Kinetic analyses of the binding of the standard R2R3 to the non-cognate DNAs and those of the R2R3 mutant proteins to the cognate DNA showed that the reduction of the binding affinity was mainly due to an increase in the dissociation rate.

Animals↗

Desmoid tumor of the chest wall following chest surgery: report of a case.

Desmoid tumors of the chest wall following chest surgery are a rare occurrence. A case of this disease is reported herein together with a review of the literature. A 74-year-old man, who had previously undergone a right lower lobectomy for squamous cell carcinoma of the lung, was referred to our hospital with an abnormal shadow on his chest X-ray. The tumor, located in the right lateral chest wall, was successfully resected by an aggressive, wide extirpation, and a final diagnosis of a desmoid tumor originating in the chest wall was made. When following up patients after surgery for lung cancer, the possibility of desmoid tumors developing in the incised chest wall should therefore be kept in mind.

Aged↗

A novel mutation, of the Bacillus subtilis hut operon that relieves both catabolite repression and amino acid repression.

A mutation, designated hutCR11, which resulted in high expression of the hut operon and release of the catabolite repression and amino-acid repression of hut expression, was isolated and determined to be a T-to-G transversion at position +30 (+1 indicates the transcription-initiation site). In the hutCR11 mutant, levels of hutP mRNA were 5-fold higher than those in wild-type cells under conditions of non-induction and induction and 11-fold higher under conditions of catabolite repression and amino-acid repression. Mutation analysis showed that two types of base change (T-->A and T-->C) at position +30 did not cause high expression of the hut operon, indicating that this was specifically caused by the single base substitution (T-->G) at position +30. The base substitution of A for T at position +30 also led to partial relief of both catabolite repression and amino-acid repression. These results indicate that the nucleotide sequence at +30 is important for regulation of both catabolite repression and amino-acid repression of the hut operon.

Bacillus subtilis↗

Can secondary degeneration accelerate the formation of neurofibrillary tangles? A case of hemispheric infarction showing asymmetric degeneration of the substantia nigra, red nuclei, inferior olivary nuclei and dentate nuclei with concomitant changes of progressive supranuclear palsy.

A case of hemispheric infarction involving the territory of the right middle cerebral artery and the thalamus showed conspicuous asymmetric degeneration in the substantia nigra, red nuclei, inferior olivary nuclei and dentate nuclei with concomitant changes of progressive supranuclear palsy (PSP). The right substantia nigra and red nucleus showed loss of neurons and proliferation of astrocytes. The right olivary nucleus was hypertrophic, while the neuronal loss and astrocytosis in the dentate nucleus were predominant on the contralateral side. Modified Gallyas-Braak staining revealed the extensive distribution of neurofibrillary tangles (NFTs), threads and intraglial argyrophilic structures in the globus pallidus, subthalamic nuclei, cerebral cortex and dentate nuclei, as well as in the affected brain stem nuclei, with a distinct predominance on the affected side. In this case, the one-sided predominance of the extended degeneration in these brain stem and cerebellar areas is considered, in addition to the PSP changes, to be due to secondary retrograde degeneration via the nigrostriatal and dentato-rubro-thalamic pathways following the hemispheric infarction, and to also be the result of disruption of the dentato-olivary fiber connections. In addition, because of the predominant distribution of NFTs on the more degenerated side, it is surmised that the formation of NFTs may be accelerated by secondary degeneration.

Aged↗

Tumor angiogenesis and recurrence in stage I non-small cell lung cancer.

BACKGROUND: Tumor angiogenesis appears to relate to recurrence after an operation as a route for distant metastasis. We assessed the association of vascular endothelial growth factor (VEGF) expression and intratumoral microvessel density (MD) with recurrence in primary lung cancer. METHODS: Samples were randomly obtained from 104 stage I lung cancer patients who underwent curative operations (43 recurrent, 61 nonrecurrent patients). Microvessels were highlighted by staining endothelial cells for factor VIII and VEGF antigen was detected using a polyclonal antibody. RESULTS: VEGF antigen was detected in large amounts in both recurrent (100%) and nonrecurrent tumors (73.8%). The percentages of patients with the strongest VEGF stain (more than 50% of staining area in tumor cells) were 46.5% in tumors with recurrence and 11.5% in tumors without recurrence. The mean MD in recurrent and nonrecurrent tumors were 18.2+/-10.5 and 8.5+/-5.0, respectively, resulting in a significantly greater value in tumors with recurrence (p<0.0001). Although there were no significant differences in mean MD according to pathological types, in adenocarcinoma and adenosquamous carcinoma, the mean value in the recurrent group was significantly greater than that in the nonrecurrent one. CONCLUSIONS: An evaluation of VEGF expression and MD in tumors may contribute to the estimation of the risk of recurrence of non-small cell lung cancer in early stages.

Adult↗

Immunosuppressant FK506 inhibits inducible nitric oxide synthase gene expression at a step of NF-kappaB activation in rat hepatocytes.

BACKGROUND/AIMS: Recent evidence indicates that an increase in nitric oxide production after liver transplantation is associated with acute allograft rejection. Nitric oxide mediates cellular injury under various pathological conditions in the liver. Studies were performed to determine whether the immunosuppressants FK506 and cyclosporin A directly influence gene expression of inducible nitric oxide synthase by interleukin 1beta in hepatocytes. METHODS: Primary cultures of rat hepatocytes were treated with interleukin 1beta in the presence and absence of FK506 or cyclosporin A. Release of nitrite (nitric oxide metabolite) into culture medium, levels of inducible nitric oxide synthase protein and mRNA, and activation of nuclear factor-kappaB were compared with the two drugs. RESULTS: Interleukin 1beta increased levels of inducible nitric oxide synthase protein and inducible nitric oxide synthase mRNA, as well as nitric oxide production, in the cultured hepatocytes. Nuclear factor-kappaB, an important transcription factor in inducible nitric oxide synthase gene expression in response to inflammation, also appeared in the nuclear fraction of hepatocytes after addition of interleukin 1beta. FK506 markedly inhibited the nitric oxide formation, inducible nitric oxide synthase protein synthesis and inducible nitric oxide synthase mRNA expression induced by interleukin 1beta, but cyclosporin A had no effects. Furthermore, FK506 inhibited nuclear factor-kappaB activation and decreased mRNA levels of the p50/p65 subunits of nuclear factor-kappaB. CONCLUSIONS: These results demonstrate that FK506, but not cyclosporin A, inhibits the induction of inducible nitric oxide synthase expression during nuclear factor-kappaB activation. FK506 may influence liver function during diseases by modulating the nitric oxide pathway, in addition to its immunosuppressive effect.

Animals↗

Neurodegeneration in hereditary nucleotide repair disorders.

Both xeroderma pigmentosum group A (XPA) and Cockayne syndrome (CS) are rare autosomal disorders, have a genetic defect in the step of nucleotide repair, and involve various neurological abnormalities caused by progressive neurodegeneration. We performed comprehensive neuropathological analysis of five cases of XPA and four cases of CS. The XPA cases showed widespread neuronal loss throughout the central nervous system, in sharp contrast to the comparative preservation of neurons in the CS cases, who rather exhibited patchy demyelination in the cerebral and cerebellar white matter, and multifocal calcium deposition in the basal ganglia and cerebral white matter, respectively. Exceptionally in the cerebellar cortex, neuronal loss was more severe in CS than in XPA. Grumose or foamy spheroid bodies occurred in the globus pallidus and substantia nigra, and axonal torpedoes were increased in the cerebellar cortex in both disorders. Neither silver impregnation nor immunohistochemistry for ubiquitin or tau succeeded in visualizing neurofibrillary tangles, senile plaques or augmented ubiquitination in either disorder, and these findings did not support the involvement of facilitated aging in the neurodegeneration in XPA or CS.

Adolescent↗

Interictal hyperperfusion observed in infants with cortical dysgenesis.

We investigated increases of interictal regional cerebral blood flow (rCBF) in patients with intractable epilepsy caused by cortical dysgenesis. Using single photon emission computed tomography, we measured interictal rCBF of epileptic foci in 24 patients with cortical dysgenesis who achieved Engel Class I or II outcomes at least 1 year after surgical intervention. The patients included 14 males and ten females, ranging in age from 2 months to 34 years (mean 6 years and 5 months). In the interictal period, dysplastic areas showed hyperperfusion in four patients (17%), hypoperfusion in 15 (62%), and isoperfusion patterns in five (21%). Interictal hyperperfusion was found in four infants aged 3-4 months; three with focal cortical dysplasia and one with hemimegalencephaly. Our results suggest that interictal hyperperfusion may indicate the presence of an active epileptic focus in infants with cortical dysgenesis, but not in older children or adults with the same disorder. Given the risk of misinterpreting the normal side as hypoperfused, the phenomenon of interictal hyperperfusion in the epileptogenic area should be taken into account when diagnosing pediatric epilepsy caused by cortical dysgenesis.

Adolescent↗

Simultaneous determination of alpha-fetoprotein, human chorionic gonadotropin and estriol in serum of pregnant women by time-resolved fluoroimmunoassay.

We have developed a simple and rapid time-resolved fluoroimmunoassay (TR-FIA) for simultaneous determination of alpha-fetoprotein (AFP), human chorionic gonadotropin (hCG) and estriol (E3) using europium and samarium ion chelate. In the proposed method, we used a combination of a 96-well microtiter plate for the AFP and hCG assay and transferable solid phase plate for the E3 assay. Therefore, these analytes could be measured simultaneously. The measurable ranges for AFP, hCG and E3 by the proposed method were 3.91-1000 ng ml(-1), 877-250000 IU l(-1) and 0.39 100 ng ml(-1), respectively. The proposed method which utilized characteristics of a rare earth ion chelate, was convenient (unnecessary diluting samples), quick (96 assays for 2 h), and required only a small quantity sample (50 microl). The principle of this proposed method is applicable to other antigens.

Antibody Specificity↗

Hematopoietic stem cell transplantation (HSCT) for Langerhans cell histiocytosis (LCH) in Japan.

There exists limited information about the usefulness of hemopoietic stem cell transplantation (HSCT) for the treatment of patients with refractory Langerhans cell histiocytosis (LCH). We report here four Japanese pediatric patients with multisystem LCH disease who underwent HSCT between 1994 and 1997. Two of the four patients are doing well without any relapse. However, neither of them shows improved sequelae 3 to 4 years after allogeneic HSCT, although the graft was rejected in one of the cases. The remaining two patients died of septic shock. A review of the literature of 11 patients revealed four fatalities after the use of HSCT in the treatment of LCH. Three of these were due to active LCH and three deaths occurred within 2 months after HSCT. To establish the usefulness of HSCT for refractory LCH, further studies are required.

Child↗