Transplantation of bone marrow cells from nonobese diabetic (NOD) mice, a model for type 1 diabetes mellitus, to C3H/HeN mice, which express I-Ea molecules and have aspartic acid at residue 57 of the I-Ap chain, induced insulitis followed by overt diabetes in the recipient C3H/HeN mice more than 40 weeks after bone marrow transplantation. When cyclosporin A, which perturbs T-ceil functions, was injected intraperitoneally into [NOD -* C3H/HeN] chimeric mice daily for 1 month, the chimeric mice developed insulitis and overt diabetes within 20 weeks following bone marrow transplantation. Transplantation of bone marrow cells from (NZW x BXSB)F1 mice, which develop lupus nephritis, myocardial infarction, and idiopathic thrombocytopenic purpura, into C3H/HeN or C57BL/6J mice induced in the recipient strains both lupus nephritis and idiopathic thrombocytopenic purpura more than 3 months after transplantation.

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SUMMARY The case of the right-handed young Japanese woman with alexia with agraphia of kanji (the Japanese morphograms) due to a small circumscribed haematoma in the left posterior inferior temporal gyrus is described. Her chief complaint was the inability to read and write kanji. Detailed examination showed that her alexia with agraphia was much more predominant for kanji than kana (the Japanese syllabograms). These facts suggest that the processing of kanji and kana involves different intrahemispheric mechanisms.Recent neuropsychological studies have revealed that the left cerebral hemisphere is responsible for the reading and writing of both kanji (which are the structurally complex morphograms in written Japanese with often several phonetic readings) and kana (which are the relatively simple syllabograms with unambiguous phonetic readings) (

The transplantation of partially purified hemopoietic stem cells (HSCs) plus the engraftment of bone from autoimmune-prone mice ((NZW × BXSB)F1 (W/BF1) mice) induces autoimmune diseases in major histocompatibility complex (MHC)-incompatible normal C3H/HeN mice. In contrast, W/BF1 mice die of infection or anemia within three weeks due to a failure in hemopoietic reconstitution when the mice receive partially purified HSCs plus bones from normal C3H/HeN mice, although they survive more than a year without showing any symptoms of autoimmune diseases when they receive T cell-depleted bone marrow cells (without bone grafts) from normal mice. This finding suggests that abnormal HSCs can proliferate even in MHC-incompatible microenvironments, while normal HSCs cannot. This is confirmed by spleen colony-forming assays (CFU-S) on day 12, using pluripotent HSCs (P-HSCs). The P-HSCs of old (> 4 mo) W/BF1 mice (after the development of autoimmune diseases) form high CFU-S counts on day 12 even in the allogeneic C3H environment, although the P-HSCs of normal mice form high CFU-S counts only in the MHC-compatible environments. In addition, abnormal P-HSCs of autoimmuneprone mice can proliferate in vitro in collaboration with MHC-incompatible stromal cells, although normal HSCs do so in collaboration with MHC-compatible stromal cells, but not MHC-incompatible stromal cells. These findings indicate that abnormal P-HSCs are more "resilient" than normal P-HSCs. Stem Cells 1997;15:56-62 STEM CELLS 1997;15:56-62Correspondence: Dr. Susumu Ikehara, 1st Department of Pathology, Kansai Medical University, 10-15 Fumizono-cho, Moriguchi City, Osaka 570, Japan. Received May 28, 1996; accepted for publication August 13, 1996. ©AlphaMed Press 1066 INTRODUCTIONThe availability of various animal models for autoimmune diseases has helped elucidate the etiopathogenesis of these diseases. We have previously found that allogeneic bone marrow transplantation (BMT) can be used to prevent insulin-dependent diabetes mellitus (IDDM), an organ-specific autoimmune disease, in nonobese diabetic (NOD) mice [1], and that the transplantation of both pancreas and BM from normal mice has a curative effect on overt diabetes in NOD mice [2]. We have also found that BMT can be used to prevent and treat systemic autoimmune diseases in BXSB [3], (NZB × NZW)F1 [4] and (NZW × BXSB)F1 [5] (W/BF1) mice; in MRL/lpr mice with abnormal radioresistant hemopoietic stem cells (HSCs), we have recently found that BMT with bone grafts (to recruit donor-derived stromal cells) prevents a relapse in autoimmune diseases [6,7], although conventional BMT fails to prevent a relapse in systemic lupus

Recent neuropsychological studies have revealed that the processing of kanji (the Japanese morphograms) and kana (the Japanese syllabograms) involves different intrahemispheric mechanisms. We describe a patient showing left unilateral agraphia without apraxia for kanji, but not for kana, who was diagnosed by magnetic resonance imaging as having a lesion of the posterior body of the corpus callosum. This patient indicates that different neural pathways are used for kanji and kana not only intrahemispherically, but also interhemispherically.