A case of aspergilloma detected after surgery for pneumothorax.

We report a case of aspergilloma in an 80-year-old male patient who had no identifiable underlying disease before surgery for pneumothorax. He was hospitalized for left pneumothorax. A chest CT revealed a large bulla in the left lung apex with a nodule (diameter; 1.5 cm) at the edge of the bulla. After thoracodocesis, air leakage persisted and a large bulla and nodule were resected. Aspergillus was detected histopathologically in the nodule. Treatment with itraconazole 200 mg a day followed, and 4 months later he had no recurrent pneumothorax or Aspergillus infection.     

Malignant lymphoma occurring subsequent to autoimmune disease]

The authors report six cases of non-Hodgkin's lymphoma (NHL) (3B-cell type, one T-cell type, one non-T non-B cell type, one unclassified type) occurring subsequently to autoimmune diseases. The patients were females aged 43 to 70 (median 61). Rheumatoid arthritis was most frequent as the preceding autoimmune disease, and the intervals from the onset of an autoimmune disease to that of NHL were 10 to 36 years (median 20). Polyclonal hypergammaglobulinemia was seen in 4 cases, lymphocytopenia in 3 cases, and conversion to negative PPD reaction in 2 cases. Only one patient had been given corticosteroids, and immunosuppressive agents may not contribute much to the development of lymphoma in patients with autoimmune diseases.     

Neuropathology of progressive multifocal leukoencephalopathy]

Progressive multifocal leukoencephalopathy (PML) is caused by opportunistic infection of JC virus which belongs to Papovavirus, and presents with progressive demyelinating lesion in the central nervous system. PML was originally reported as a rare complication of hematologic disorders, but later greatly increased in number in association with acquired immunodeficeincy syndrome (AIDS). Original neuropathological features of PML consist of demyelination lacking inflammatory reaction or necrosis, accompanying oligodendroglial nuclear inclusions in the periphery of demyelination. The lesion is preferentially localized to gray-white junction of the cerebral hemisphere and manifests as characteristic demyelinating lesion, called scallopping. Detection of JC virus is essential for the final diagnosis of PML and is achieved via immunohistochemical detection of JC virus with antibodies raised against their components, ultrastructural demonstration of virions characteristic of JC virus, or detection with in-situ hybridization of the genome of JC virus. JC virus can replicate only in oligodendroglial cells, but astrocytes are frequently infected by the virus. The resume of immunological function through therapeutic intervention develops new pathology in PML, exhibiting severe inflammatory reaction with edema and necrosis. This new pathological feature is called immune reconstruction syndrome and clinically presents with severe progression in symptoms of the central nervous system. Nevertheless, treatment of PML is directed for the elimination of the viruses by host immune system. The modification of the above immune reconstruction syndrome is essential for successful outcome of such therapeutic trial.     

Comparison of transfer and distribution of technetium and rhenium in radish plants from nutrient solution

Tracer experiments were carried out to compare the plant uptake behavior of Tc and Re from nutrient solutions. Radish plants, transplanted to nutrient solution including various tracers, showed the same uptake and distribution of ^95mTc and ¹⁸³Re. The trend was the same when the ⁹⁹Tc and stable-Re concentrations were increased in nutrient solution. The behavior of other elements was different from that of Tc and Re. These findings suggest the possible use of Re as the chemical analogue of Tc in soil solution to plant uptake experiments.     

Methylmercury causes diffuse damage to the somatosensory cortex: how to diagnose Minamata disease]

The first acute case of methylmercury (MeHg) poisoning by the consumption of fish arose in Minamata, Japan, in 1953. It was officially recognized and called Minamata disease (MD) in 1956. There are still arguments about the definition of MD in terms of its associated clinical symptoms and lesions even 50 years after the initial recognition of MD. Studies on this MD epidemic are reviewed along with its historical background. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea had been exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These chronic MeHg poisoning patients complained of paresthesia at the distal parts of their extremities and around the lips even 30 years after the cessation of exposure to MeHg of anthropogenic origin. The persisting somatosensory disorders after the discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed. Based on these findings, symptoms and lesions in MeHg poisoning are reappraised.     

Phenotypic and Genotypic Lineage Switch of a Lymphoma with Shared Chromosome Translocation and T-Cell Receptor γ Gene Rearrangement

A case of non-Hodgkin's lymphoma showed a phenotypic and genotypic cell lineage switch twice during nine years of his clinical history; first, T-cell type, pleomorphic small cell lymphoma developed, followed by B-cell type, diffuse centroblastic/centrocytic lymphoma, and finally T-zone lymphoma without follicles again developed, from which AST-1 cultured cell line was established. Karyotype analysis demonstrated a shared abnormal chromosome, der(1)t(1;?)(p36;?), among the first relapsed B-cell tumor, the second relapsed T-cell tumor and AST-1 cell line. Furthermore, T-cell receptor (TCR) γ gene rearrangement bands of the same size were observed in the first relapsed B-cell tumor and the second relapsed T-cell tumor as well as AST-1 cell line. These results suggested that both relapsed tumors of different cell lineages are derived from a common malignant clone, presumably a committed lymphoid stem cell. A unique translocation, t(2;14)(q37;q11.2), which may involve TCR δ/α gene complex, was observed in the second relapsed tumor and AST-1 cells. To attempt to isolate the breakpoint of this translocation, the configuration of TCR δ/α gene complex was studied. The result showed that two rearrangements of TCR α gene detected with J_α probes were the products of the normal TCR rearrangement process, and were not involved in the translocation at this region. This patient, together with the AST-1 cell line, provided us a unique opportunity to study the development and clonal evolution of malignant lymphoma.     

Histamine metabolism in the nasal tissue of human and nasal hypersensitive guinea-pig

Histamine (HA) is the most important mediator of nasal allergy and nasal hypersensitivity. To investigate HA metabolism, HA content and activities of its synthetic enzyme, histidine decarboxylase (HDC) and degrading enzymes, histamine-N-methyltransferase (HMT) and diamine oxidase (DAO) in nasal mucosa of human and toluene diisocyanate (TDI) sensitized guinea-pigs were measured. In human nasal mucosa and nasal polyps, HA content and HDC activity were 80-200 nmol/g tissue, 20-30 fmol/min/mg protein respectively. Among two degrading enzymes, HMT activity was 20-200 times higher than that of DAO. In the nasal mucosa of guinea-pigs, HA content was significantly increased by TDI sensitization, and was decreased immediately after TDI provocation. In 24 hours after provocation, HA content recovered to 80% of pre-provocation level. HDC activity increased by TDI sensitization significantly. Though HMT activity increased slightly by TDI sensitization and provocation, DAO activity was unchanged. The data suggest that, increase in turnover rate of HA is present in allergic nasal mucosa.     

Conditions of Alzheimer-type dementia in the old-old and oldest-old patients with special reference to extreme conditions of brain aging

A neuropathological study on 1540 consecutive autopsy brains ranging from 60 to 107 years of age revealed the following points. (1) Of the of the demented cases of the plaque-predominant type, 93% were complicated with multiple tiny cortical infarcts. They showed a tendency for dementia to develop before or after the appearance or worsening of a systemic disorder such as cardiovascular disease, respiratory infection and cancer. However, there was no case showing Alzheimer-type dementia (ATD). (2) The plaque-predominant type might be an extreme condition of brain aging in terms of senile plaques (SP). It is likely that although the pathological appearance of SP alone is not responsible for dementia, its coexistence with multiple cortical infarcts could be the cause of dementia. Therefore, this type should be distinguished from ATD. (3) Primary hippocampal degeneration could also be an extreme condition of brain aging in terms of neurofibrillary tangles. This condition was different pathologically from the hippocampal lesion in ATD. (4) Several characteristics of old-old and oldest-old patients were clarified.