Eosinophils are one of the inflammatory cells involving allergic diseases and are recognized as effector cells in airway inflammation of bronchial asthma. The two major effector functions are the release of toxic granule proteins and active oxygen species. Here we examined the effects of toxic granule proteins of human eosinophils, such as major basic protein (MBP), eosinophil peroxidase (EPO), eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN) against airway lung carcinoma cells (A549 cell, ATCC CCL185) which were infected with respiratory syncytial virus (RSV). Cytopathic effects of A549 cells were observed in the course of time (every 24 hour). None of injury on A549 cells was observed in cases of RSV alone whose dose was 0.1 and 1 moi up to 48 hours. High concentrations of MBP and EPO did harm to A549 cells by themselves after 24 hours, however ECP and EDN didn't such response even after 48 hours in macro phase. On the other hand, in case of infection with RSV, the degree of injury in A549 cells treated with MBP and EPO was significantly increased; it depended on the concentration of RSV in macro phase. The viability of A549 cells which were infected and/or treated were also measured by the cell viability analyzer (Vi-CELL). It exhibited that the viability of A549 cells which were infected with RSV and following treated with eosinophil granule proteins was lower than that of RSV infection alone. The results suggested that eosinophils and its products might induce excess injury to airway epithelial cells especially when airway epithelial cells were infected with RSV and this might promote the eosinophilic inflammation in bronchial asthma.

We performed flow cytometric and ultrastructural studies of pure erythroid leukemia (M6b) with carbonic anhydrase I (CA I) expression. A total of fifteen patients (mean age 46 years, range 1 to 85 years) were examined. The initial diagnoses were chronic myeloid leukemia in two, myelodysplastic syndrome in nine including four cases of Down syndrome, pancytopenia or bicytopenia in three, and myelofibrosis in one. Flow-cytometrically, almost all tumor cells were positive for CD36. CD4 and CD7 (T-cell markers), as well as CD13 and CD33 (panmyeloid markers) were also expressed in more than 90% of cases. Blood type antigens were also positive in 8 of 10 cases. CD34, CD117 and HLA-DR (immature myeloid markers) were also expressed in approximately 80% of cases. Other positive myeloid markers were CD45RA (7/13, 54%), CD11b (5/12, 42%) and CD45RO (9/13, 69%). Blast cells were positive for CD41, 61, 42a and 42b (megakaryocytic markers) in 60% of cases, but CD235a (specific marker for erythroid cells) was expressed in 7 of 15 cases (47%). Electron microscopic studies of platelet peroxidase (PPO) reaction revealed that in five of fourteen cases a very small number of tumor cells showed positive reaction. In conclusion, to make diagnosis of M6b, investigation of erythroid markers are mandatory, because tumor cells of M6b showed variable antigens, such as CD4, 7, 13, 33, 34, 36, 41, 42b, 61, 117, HLA-DR and PPO. CD36 is suitable for screening erythroid lineage marker, and blood type antigens and CA I are specific antigens for M6b besides CD235a.

Human telomerase reverse transcriptase (hTERT) is the catalytic subunit of telomerase, which is highly active in immortalized cells and most of human cancers but is quiescent in most normal somatic cells. Using a binary adenovirus system that can induce Bax gene expression, we showed that induction of Bax gene expression via the hTERT promoter elicited tumor-specific apoptosis in vitro, suppressed tumor growth in nude mice, and prevent the toxicity of Bax gene in vitro and in vitro. We constructed a tumor-specific replication-competent adenovirus, in which the hTERT promoter element drives expression of E1A and E1B genes. TRAD induced selective E1A and E1B expression in human cancer cells, but not in normal cells. TRAD replicated efficiently and induced marked cell killing in cancer cell lines,whereas replication as well as cytotoxicity was highly attenuated in normal human fibroblasts. In nu/nu mice carrying s.c. human lung tumor xenografts, intratumoral injection of TRAD resulted in a significant inhibition of tumor growth. No evidence of TRAD was identified in tissues outside of the tumors, despite the presence of TRAD in the circulation. Moreover, TRAD replication in the distant, non-injected tumors was demonstrated.

Spinal cord injury (SCI) has been considered to be irreversible. However, this is not true. There has been remarkable progress in the basic research of new treatments for SCI. In this article, we review these paths,and highlight the possibility that these experimental strategies can be applied to clinical medicine. Especially we discuss recent progress in the effect of treatments using bone marrow stromal cells (BMSCs) on SCI. And we present our recent studies concerning with BMSCs transplantation for SCI rats in vivo and the capacity of BMSCs to differentiate into neural stem like cells in vitro. In vivo study, we demonstrate that few BMSCs can differentiate into neural like cells, but functional recovery resulted from BMSCs treatment. In vitro study, we demonstrate our original cell operation methods of induction from BMSCs into neurospheres. It is our hope that further understanding of the mechanisms underlying functional recovery will lead to therapeutic strategies in humans. Less than 10% of the axons of the spinal cord can support substantial function, I believe that the therapeutic application of BMSCs and unique cells origin for BMSCs will lead SCI patients to return to walk again.