Development of invasive adenocarcinoma in a long-standing diverted ileal J-pouch for ulcerative colitis

We report a case of a 50-year-old male with ulcerative colitis who developed well-differentiated adenocarcinoma in the ileal J-pouch, which had been defunctioning for 18 years. The extension of the carcinoma in the pouch suggested that it had recently appeared in the pouch. Monitoring by endoscopic examination and biopsy or pouch excision seems to be an appropriate action if a pouch is out of the fecal stream.     

Hematological study on a case with cerebellar hemangioblastoma associated with erythrocytosis,with special reference to a erythropoiesis-stimulating activity present in the fluid of the cyst of tumor

Summary A case of cerebellar hemangioblastoma associated with slight but definite erythrocytosis is reported. Operative removal of the tumor resulted in the reversion to a normal blood picture. Erythropoietin-like activity, being non-dialyzable and relatively thermolabile, was detected in the fluid aspirated from tumor. The mother of the reported patient suffered from the same disease which was also associated with a slight degree of erythrocytosis.

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Zusammenfassung Es wird über den Fall eines cerebellaren Hämangioblastoms begleitet von einer leichten, aber doch eindeutig diagnostizierten Erythrozytose berichtet. Die operative Entfernung des Tumors führte zu einer Renormalisierung des Blutbildes. In der aus dem Tumor aspirierten Flüssigkeit wurde eine erythropoetinähnliche Wirkung entdeckt, die relativ thermolabil und nicht dialysierbar war. Die Mutter des geschilderten Patienten litt an der gleichen Krankheit, die ebenfalls von einer Erythrozytose leichten Grades begleitet war.

     

A mitochondrial superoxide theory for oxidative stress diseases and aging

Fridovich identified CuZnSOD in 1969 and manganese superoxide dismutase (MnSOD) in 1973, and proposed ”the Superoxide Theory,” which postulates that superoxide (O₂^•−) is the origin of most reactive oxygen species (ROS) and that it undergoes a chain reaction in a cell, playing a central role in the ROS producing system. Increased oxidative stress on an organism causes damage to cells, the smallest constituent unit of an organism, which can lead to the onset of a variety of chronic diseases, such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis and other neurological diseases caused by abnormalities in biological defenses or increased intracellular reactive oxygen levels. Oxidative stress also plays a role in aging. Antioxidant systems, including non-enzyme low-molecular-weight antioxidants (such as, vitamins A, C and E, polyphenols, glutathione, and coenzyme Q₁₀) and antioxidant enzymes, fight against oxidants in cells. Superoxide is considered to be a major factor in oxidant toxicity, and mitochondrial MnSOD enzymes constitute an essential defense against superoxide. Mitochondria are the major source of superoxide. The reaction of superoxide generated from mitochondria with nitric oxide is faster than SOD catalyzed reaction, and produces peroxynitrite. Thus, based on research conducted after Fridovich’s seminal studies, we now propose a modified superoxide theory; i.e., superoxide is the origin of reactive oxygen and nitrogen species (RONS) and, as such, causes various redox related diseases and aging.     

Contribution of increased minimal coronary resistance and attenuated vascular adaptive remodeling to myocardial ischemia in patients with systemic hypertension and ventricular hypertrophy

This study assessed the impact of coronary vascular adaptive remodeling and coronary vascular reactivity on myocardial ischemia in patients with hypertension and left ventricular hypertrophy. Myocardial ischemia is associated with impaired endothelium-independent vasodilation of resistance coronary arteries and increased minimal coronary resistance. These changes may occur in association with lumen reduction caused by attenuated adaptive remodeling in response to plaque accumulation.     

Acute myeloid leukemia originating from the same leukemia clone after the complete remission of acute lymphoid leukemia

A 22-year-old female was diagnosed as having acute lymphoid leukemia (ALL) in February 1995, from the findings of peroxidase negative, CD10+, CD19+, TdT+ and rearrangement of IgH and TCR beta. AdVP (doxorubicin, vincristine and prednisolone) therapy achieved a complete remission (CR). Bone marrow transplantation had to be abandoned because of the lack of an HLA-identical donor. Intensification therapy was thus carried out repeatedly. In June 1998, myeloblast with Auer rods, peroxidase positive, CD13+, CD33+ and HLA-DR+, appeared. The patient was diagnosed as having lineage switch acute myeloid leukemia (AML) from ALL. Though A-DMP (cytosine arabinoside, daunorubicin, 6-mercaptopurine) therapy was resistant, AdVP therapy led to a CR. The patient died of cardiotoxicity from anthracyclines in February 1999. From the results of the Ramasamy method using the clonal rearrangements of the Ig heavy chain gene locus, the origin of the pathological cells of ALL and AML was indicated to be the same leukemia clone.