Biomedical subjects

Yuji Ohtsuki

Publications and source records attributed to Yuji Ohtsuki.

84 records · Page 5Linked to original sources

PubMed2002

A study on intraalveolar exudates in acute mycoplasma pneumoniae infection.

Pathologic features of Mycoplasma pneumoniae infection (M. pneumonia) are generally non-specific, and the literature regarding the pathologic features of M. pneumonia with intraalveolar exudates is limited. Clinical and histopathological studies were performed in 3 patients with M. pneumonia which did not respond to erythromycin and minocycline, but all rapidly recovered after corticosteroid therapy. In pathologic findings, we observed intraalveolar exudates and focal organization in M. pneumonia, and its intraalveolar lesions were compared between M. pneumonia and bronchiolitis obliterans organizing pneumonia containing fibrin (BOOP). Immunohistochemical studies were performed using the streptavidin biotin peroxidase complex method with anti-alpha-smooth muscle actin antibody and anti-pancytokeratin AE1/AE3 antibody. In pathologic findings, more fibrin deposits in intaalveolar lesions were observed in M. pneumonia than in BOOP. In intaalveolar lesions of M. pneumonia, a larger amount of nuclear debris, more neutrophils, and more erythrocytes were noted. Myofibroblasts were observed in the organization of BOOP, while in the intaalveolar lesions of M. pneumonia, myofibroblasts were not observed. These results suggest that M. pneumonia with intraalveolar exudates responds well to corticosteroid and its intraalveolar lesions apparently differed from those in BOOP.

Acute Disease↗

PubMed2002

Occurrence of bronchioloalveolar cell carcinoma in two brothers: comparison of clinical features and immunohistochemical findings.

It has been suggested that lung cancer sometimes aggregates in families. However, the familial occurrence of bronchioloalveolar carcinoma (BAC) is extremely rare. We present a family in which two brothers had BAC. The clinical features and immunohistochemical findings of BAC in the two brothers were compared. Immunohistochemical findings revealed that both cases of BAC had very similar immunopathological features in epithelial marker expression. A review of the literature revealed that this is the third case of BACs in a single family.

Adenocarcinoma, Bronchiolo-Alveolar↗

PubMed2002

Pathological analysis of the cavitary wall in Mycobacterium avium intracellulare complex pulmonary infection.

OBJECTIVE: The present study was designed to evaluate the process of cavity formation in Mycobacterium avium intracellulare complex (MAC) lung infection, pathologically and clinically. METHODS: Using resected lung specimens, we first evaluated the distribution of MAC as well as the distribution of myofibroblasts in MAC lung infection according to several pathological findings classified as bronchiectasis, centrilobular nodules, cavity, nodules, bronchiolitis, or consolidation. Resected lung specimens (9 cases) were evaluated by special staining: Ziehl-Neelsen's method and immunohistochemically for CD68 (stain for monocytes and macrophages) and alpha-smooth muscle actin (stain for myofibroblasts). Chest CT findings were also examined in these 9 patients. In addition, the serial chest CT scans were reviewed in another 3 patients to evaluate the process of cavity formation, radiologically. RESULTS: Although extensive granuloma formations were observed in every pathological classification, MAC was demonstrated only in the necrotic tissue of the inner surface of the cavitary wall, which was connected to the airway. Myofibroblasts which expressed alpha-smooth muscle actin were intensely demonstrated in the cavitary wall compared with other pathological classifications. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and the layer of myofibroblasts surrounded the layer of epithelioid cells. Chest CT findings demonstrated that the cavitary walls were relatively thick. The evaluation of serial chest CT scans demonstrated that cavities were formed from previously existing nodules. CONCLUSIONS: Detection of mycobacteria in the cavitary wall, massive infiltration of myofibroblasts compared with other pathological classifications, and connection to the drainage bronchus, were believed to be important in the process of cavity formation in MAC pulmonary infection.

Adult↗

PubMed2002

Nonspecific interstitial pneumonia/fibrosis completely recovered by adding cyclophosphamide to corticosteroids.

Nonspecific interstitial pneumonia/fibrosis (NSIP) was first described by Katzenstein and Fiorelli in 1994 (Am J Surg Pathol 18: 136-147). Many reports have described that corticosteroids are effective for NSIP. We describe a case of group II idiopathic NSIP in whom cyclophosphamide was administered since the initial response to corticosteroids had been insufficient. Lung biopsy was performed by video-assisted thoracoscopic surgery and NSIP was diagnosed pathologically, clinically and radiologically. Although the initial response to corticosteroids was insufficient, interstitial infiltrates on chest computed tomography improved dramatically after adding intravenous cyclophosphamide followed by oral cyclophosphamide. This case demonstrates that the addition of cyclophosphamide to corticosteroids might be a useful treatment for patients with NSIP.

Cyclophosphamide↗

PubMed2002

Cigarette smoke-induced acute eosinophilic pneumonia accompanied with neutrophilia in the blood.

Smoking causes various changes in the lung. This report describes a case of cigarette smoke-induced acute eosinophilic pneumonia (CS-AEP) with neutrophilia in the blood. However, the precise mechanism is unknown, so we examined the effect of exposure to cigarette smoke extracts on the production of interleukin (IL)-4, IL-5, IL-8, IL-18, granulocyte macrophage-colony stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF) by human bronchial epithelial cells (HBECs) obtained from the patient. We found that IL-8 released from HBECs was involved in neutrophilia in the blood, and is a new factor in the development of AEP, especially in the early phase.

Acute Disease↗

PubMed2002

Expression of cytokeratin 19 in human hepatocellular carcinoma cell lines.

It has been reported that the cytokeratin 19 (CK19) fragment, CYFRA 21-1, is increased in sera of some hepatocellular carcinoma patients. We hypothesized that CYFRA 21-1 might be released directly from hepatocellular carcinoma. To investigate this mechanism, we evaluated expression of CK19 in 8 human cell lines by immunoradiometric assay, Western blotting, immunohistochemistry, and reverse transcriptase-polymerase chain reaction in Chang liver cells, 2 cholangiocarcinoma cell lines, and 5 hepatocellular carcinoma cell lines. Three of 5 hepatocellular carcinoma cell lines released CYFRA 21-1, synthesized CK19 protein and expressed mRNA for CK19, as observed in 2 cholangiocarcinoma cell lines. In contrast, there was no expression of CK19 in Chang liver cells or 2 of 5 hepatocellular carcinoma cell lines. Analysis of genomic DNA for CK19 demonstrated that exon 1 was not amplified in the 3 cell lines not expressing CK19. However, there were no point mutations within exon 1 and the promoter region of CK19 in hepatocellular carcinoma cell lines. Our present study demonstrates that: i) the expression of CK19 was evident in some human hepatocellular carcinoma cell lines, and ii) the expression of mRNA for CK19 was related to the release of CYFRA 21-1. These results partially clarify the mechanism by which some hepatocellular carcinoma cell lines produce CK19 and others do not.

Antigens, Neoplasm↗

PubMed2002

p53 mutation arising in Arg72 allele in the tumorigenesis and development of carcinoma of the urinary tract.

PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53. Furthermore, the Arg72-containing allele is preferentially mutated and retained in various human tumors, suggesting that polymorphic residue within p53 modifies mutant behavior. We studied to determine whether Arg72 could be a risk factor for p53 mutations in human transitional cell carcinomas (TCCs). In addition, the relationship between the status of p53 codon 72 polymorphism and clinicopathological factors of this tumor were also analyzed. EXPERIMENTAL DESIGN: We analyzed the correlation between the p53 mutations and genotypes of its codon 72 using genomic DNAs from the TCCs by direct DNA sequencing. Loss of heterozygosity was determined using a p53 microsatellite marker (TP53) amplified by PCR. RESULTS: There was a bias to mutate and express the Arg allele in the p53 -mutated TCCs arising in individuals with heterozygosity (Pro/Arg). The Arg72-containing allele was preferentially retained in these tumors. The prevalence of cases with p53 mutations within Arg72-containing allele was higher for advanced-stage TCCs (chi(2) = 5.320, P = 0.021) than for TCCs with those arising in Pro72-containing allele. CONCLUSIONS: Our in vivo findings suggested that p53 mutation alleles containing Arg72 are preferentially selected during tumorigenesis and affect mutant behavior in TCCs, and revealed that TCCs with p53 mutation arising in Arg72-containing allele became progressively more abundant with increase in tumor stage.

Aged↗

PubMed2002

[A case of pulmonary carcinomatous lymphangiosis exhibiting multiple patchy opacities, caused by CA 19-9 producing metastatic stomach cancer].

A 64-year-old man was admitted to our hospital complaining of Hugh-Jones II dyspnea. Chest CT showed multiple diffuse patchy shadows in both lung fields. A diagnosis of pulmonary carcinomatous lymphangiosis was made on the basis of the presence of adenocarcinoma cells within the lymphatic vessels in transbronchial lung biopsy (TBLB) specimens. The primary site was a tumor in the stomach. It is very rare for pulmonary carcinomatous lymphangiosis to show multiple patchy shadows in CT. Tumor cells were positive for CA 19-9. There were high titers of carbohydrate antigens, SPAN-1, CA 19-9, SLX, CA 125 and CA 724 both in the bronchial alveolar fluid (BALF) and in the serum. SPAN-1, CA 19-9 and SLX titers were higher in the BALF than in the serum. In this case, liver metastasis had also occurred with carcinomatous lymphangiosis. This case is very interesting in that type I and II carbohydrate antigens were correlated with blood-borne metastasis.

Adenocarcinoma↗

PubMed2001

SYT associates with human SNF/SWI complexes and the C-terminal region of its fusion partner SSX1 targets histones.

A global transcriptional co-activator, the SNF/SWI complex, has been characterized as a chromatin remodeling factor that enhances accessibility of the transcriptional machinery to DNA within a repressive chromatin structure. On the other hand, mutations in some human SNF/SWI complex components have been linked to tumor formation. We show here that SYT, a partner protein generating the synovial sarcoma fusion protein SYT-SSX, associates with native human SNF/SWI complexes. The SYT protein has a unique QPGY domain, which is also present in the largest subunits, p250 and the newly identified homolog p250R, of the corresponding SNF/SWI complexes. The C-terminal region (amino acids 310-387) of SSX1, comprising the SSX1 portion of the SYT-SSX1 fusion protein, binds strongly to core histones and oligonucleosomes in vitro and directs nuclear localization of a green fluorescence protein fusion protein. Experiments with serial C-terminal deletion mutants of SSX1 indicate that these properties map to a common region and also correlate with the previously demonstrated anchorage-independent colony formation activity of SYT-SSX in Rat 3Y1 cells. These data suggest that SYT-SSX interferes with the function of either the SNF/SWI complexes or another SYT-interacting co-activator, p300, by changing their targeted localization or by directly inhibiting their chromatin remodeling activities.

Amino Acid Sequence↗

PubMed1999

Ultrastructure of Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 (HHV-8) in a primary effusion lymphoma cell line treated with tetradecanoyl phorbol acetate (TPA).

The ultrastructure of Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus-8 (HHV-8) has not yet been fully elucidated, although some findings have been reported using primary effusion lymphoma (PEL) cell lines, KS-1, harboring no Epstein-Barr virus (EBV) coinfection. In the present study, detailed fine structural examination of KSHV/HHV-8 was performed after stimulation of the PEL-derived cell line KS-1 with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in vitro. While unstimulated KS-1 cells contained a small number of intranuclear virus particles associated with no extracellular mature particles, KS-1 cells stimulated with TPA produced many extracellular mature particles as well as intranuclear particles, in addition to interesting tubulo-reticular structures and aggregated tubular structures in vesicles. The induced intranuclear particles were empty, doughnut shaped, and dense cored, with outer and inner diameters of 100-110 nm and 60-70 nm, respectively. Dense-cored extracellular mature particles were 150-160 nm in diameter, and some contained doughnut-shaped cores, together with a few megaloviruses, 260 nm in outer diameter. These findings indicate that KS-1 cells treated with TPA can produce extracellular mature particles as well as intranuclear particles, which were proven to be KSHV/HHV-8.

Journal Article↗

PubMedDate not supplied

Infiltrations of Epstein-Barr virus-carrying cells in granular lymphocyte-proliferative disorders corresponding to chronic active Epstein-Barr virus infection.

A 21-year-old man with granular lymphocyte-proliferative disorders (GLPD) associated with chronic active Epstein-Barr virus (EBV) infection is described. Chromosomal analyses revealed several clonal abnormalities and two of them were mainly repetitious. High copy numbers of monoclonal EBV genome were also detected in the proliferative large granular lymphocytes (LGLs), indicating the monoclonal expansion of EBV-infected LGLs. The patient had an indolent course for several years, and there was no evidence of infiltrations of his bone marrow until the end stage. At autopsy, microscopic studies revealed marked infiltrations of LGL in the liver and spleen, and the infiltrating cells were NK-cell immunophenotype. The infiltrated LGLs showed latency I.

Adult↗

PubMedDate not supplied

Diffuse micronodular pulmonary metastasis of lung adenocarcinoma predicts gefitinib response in association with epidermal growth factor receptor mutations.

Female, non-smoker, Asian ethnicity and adenocarcinoma histology are the major clinical predictors of gefitinib response in non-small cell lung cancer, as shown in previous studies. Recently, response to gefitinib has been associated with epidermal growth factor receptor (EGFR) mutations. Higher rates of mutation were seen in females, patients with adenocarcinomas, the Asian population and never-smokers, which may explain the clinical response predictors. The presence of diffuse micronodular pulmonary metastasis on chest imaging as a novel clinical predictor of its response is proposed here. Two cases of lung adenocarcinomas in men presenting with diffuse micronodular pulmonary metastasis were encountered. Both patients showed a major response to gefitinib. The dramatic reduction of micronodular pulmonary nodules throughout both lungs on computed tomography scans was achieved after treatment for a couple of months with 250 mg of oral gefitinib. In the molecular analysis, one patient had a heterozygous delL746-A750 mutation and the other had a heterozygous L858R EGFR mutation. In conclusion, patients with lung adenocarcinoma, even men, who presented with bilateral diffuse micronodular metastatic spread to the lungs tended to have an activated EGFR mutation. Therefore, they are most likely to receive benefits from molecular target drugs such as gefitinib and possibly erlotinib.

Adenocarcinoma↗