Taizo Fukumoto

Pleuropulmonary Blastoma: Fluorescence In Situ Hybridization Analysis Indicating Trisomy 2

We report a case of pleuropulmonary blastoma occurring in the right upper lobe and pleura of a 29-month-old boy. Histologically, the tumor was composed of undifferentiated mesenchymal cells with occasional rhabdomyoblastic and chondroid differentiation. Immunohistochemical analysis showed vimentin immunoreactivity in most of the tumor cells, myoglobin, desmin, and actin in the rhabdoid cells, and S-100 protein in the chondroid cells. Fluorescence in situ hybridization (FISH) analysis showed trisomy 2 and normal chromosomal copy numbers for chromosomes 7, 12, 17, 18, and X in the majority of the tumor cell nuclei. The identification of trisomy 2 in the current pleuropulmonary blastoma confirms a previous cytogenetic finding of chromosome 2 abnormality with cultured metaphase cells of a similar case, indicating that the acquisition of an additional chromosome 2 copy in pleuropulmonary blastoma is a nonrandom chromosomal alteration and that pleuropulmonary blastoma is cytogenetically distinct from pulmonary blastoma in which chromosome 2 is bisomic. It is also suggested that pleuropulmonary blastoma may have an intimate tumorigenetic relationship with embryonal rhabdomyosarcoma.

Difference in cytokine production in acute and chronic rejection of rat lung allografts

Abstract  In Brown Norway to Lewis rat lung transplantation, short‐term administration of cyclosporine produces permanent adoption of allografts; however, the adopted grafts show symptoms of chronic rejection. To clarify the difference in cytokine production in acute an chronic rejection of the allografts, an immu‐nohistochemical study was performed. In acute rejection, positive cells for respective cytokines were observed in infiltrating cells, increasing in number as the days after transplantation passed, and reaching a maximum on the fifth day. The strongest reactivity was observed perivenously. In chronic rejection, TNF‐α positive cells were observed in the perivascular and peribron‐chial regions, especially around class II positive epithelia. The number of positive cells was, however, less than that in the vascular phase of acute rejection. Few cells were positive for IL‐lβ, IFN‐γ and, unexpectedly, for IL‐4. These facts indicate the functional difference of infiltrating cells between acute and chronic rejection.

Management of postpneumonectomy syndrome by intrapleural injection of sulfur hexafluoride

Left postpneumonectomy syndrome was managed by injection of sulfur hexafluoride (SF6) into the pleural space. This measure permitted irradiation of a contralateral, second primary lung cancer without resulting pulmonary fibrosis. Such use of SF6 may be an option for prophylaxis against postpneumonectomy syndrome.

Mediastinal esophageal cyst causing unilateral hyperlucent lung

Unilateral emphysema secondary to bronchial obstruction by a foregut-derived mediastinal cyst is rare. Here we describe an infant with a unilateral hyperlucent lung due to compression on the left main bronchus by an esophageal cyst, visualized by chest computed tomography and magnetic resonance imaging. A chest roentgenogram and a perfusion scan presented the normalized left lung after resection of the cyst.

Pleural‐changes in the lung allograft during acute rejection

Abstract To ascertain the cause of pleural fibrosis in lung allografts, pleural changes were investigated in rat syngeneic and allogeneic lung grafts. The pleura of lung syngeneic grafts showed no pathological changes except for mild edema on the first day after transplantation. In lung allografts, recipient cells migrated into the subpleural tissue early after transplantation (latent phase). In the vascuar phase, recipient lymphocytes in the subpleural tissue increased in number, while almost all alveolar structures were free from infiltration. Both CD4‐positive and CD8‐positive cells infiltrated in almost equal numbers with macrophages. The subsets of infiltrating cells were similar to those of the perivascular and peribronchial areas. In the late vascular or alveolar phase, fibro‐blasts were observed among the infiltrating cells, and fibrotic changes started. In the destructive phase, collagen formation with marked pleural thickening was dominant. Pulmonary acute rejection should be treated at least up to the late vascular phase to prevent pleural fibrosis.