Effects of High-Dose Cyclophosphamide on Ultrastructural Changes and Gene Expression Profiles in the Cardiomyocytes of Mice.

The pathogenesis of cyclophosphamide (CY)-induced cardiotoxicity remains unknown, and methods for its prevention have not been established. To elucidate the acute structural changes that take place in myocardial cells and the pathways leading to myocardial damage under high-dose CY treatments, we performed detailed pathological analyses of myocardial tissue obtained from mice subjected to a high-dose CY treatment. Additionally, we analysed the genome-wide cardiomyocyte expression profiles of mice subjected to the high-dose CY treatment.

Erythroblast predominance without CD41/cyCD41-positive blasts predicts favorable prognosis in patients with myelodysplastic syndromes and acute myeloid leukemias treated with azacitidine.

This study examined the prognostic impact of erythroblast predominance (EP) in 61 patients with myelodysplastic syndromes (MDS) (n = 51) or acute myeloid leukemia (n = 10) treated with azacitidine. Median age was 78 years. EP, defined as > 40% erythroblasts and M/E < 1.

Novel AP3B1 compound heterozygous mutations in a Japanese patient with Hermansky-Pudlak syndrome type 2.

Hermansky-Pudlak syndrome type 2 (HPS2) is an extremely rare autosomal recessive inherited disease characterized by partial oculocutaneous albinism (OCA), bleeding diathesis due to a storage pool deficiency and immunodeficiency. The disorder is caused by disruption of the adapter protein 3 complex, which is involved in impaired intracellular vesicle transport. Here, we report the first case of a 1-year-old girl with HPS2 in Asia.

RUNX1-EVI1 induces dysplastic hematopoiesis and acute leukemia of the megakaryocytic lineage in mice.

The RUNX1-EVI1 gene generated by the t(3;21) translocation encodes a chimeric transcription factor and is a causative gene in the development of de novo acute megakaryoblastic leukemia and leukemic transformation of hematopoietic stem cell tumors. Heterozygous RUNX1-EVI1 knock-in mice die in utero due to hemorrhage in the central nervous system and spinal cord and complete abolishment of definitive hematopoiesis in the fetal liver. On the other hand, the chimeric knock-in mouse develops acute megakaryoblastic leukemia.

[Quality Management of Pre-Testing Step of POCT].

To maintain a trusting relationship between clinical and hospital laboratory staff, highly reliable reporting based on precise quality control of the test results is required. Testing work is divided into 3 steps: pre-testing, testing, and post-testing. Quality control (QC) of laboratory testing has been performed to improve the precision and accuracy of measurements after sample collection, mainly in the testing step.

[Problems of self-monitoring of blood glucose (SMBG) and right drawing blood methods--the impact that technique at the time of the blood glucose self puncture drawing blood and part give measurements].

Devices for self monitoring of blood glucose (SMBG) are used by diabetic patients themselves. Evaluation of the environmental temperature during use by patients showed the importance of the temperature environment. When measurement is performed at a temperature outside the measurement temperature range, a function to display errors or does not display measurement values is indispensable.

Dysplastic definitive hematopoiesis in AML1/EVI1 knock-in embryos.

The AML1/EVI1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/EVI1 chimeric gene into mouse Aml1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/EVI1/+ embryo showed defective hematopoiesis in the fetal liver and died around embryonic day 13.

AML-1 is required for megakaryocytic maturation and lymphocytic differentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis.

Embryonic development of multilineage hematopoiesis requires the precisely regulated expression of lineage-specific transcription factors, including AML-1 (encoded by Runx1; also known as CBFA-2 or PEBP-2alphaB). In vitro studies and findings in human diseases, including leukemias, myelodysplastic syndromes and familial platelet disorder with predisposition to acute myeloid leukemia (AML), suggest that AML-1 has a pivotal role in adult hematopoiesis. However, this role has not been fully uncovered in vivo because of the embryonic lethality of Runx1 knockout in mice.

Polycystic kidney and renal cell carcinoma in Japanese and Chinese toad hybrids.

Frequent development of renal cell carcinomas in hybrids between Japanese toads (Bufo japonicus) and imported Chinese toads (Bufo raddei) was first reported by 2 of our authors in 1987. Such renal tumors of toads had never been observed previously in the laboratory. To confirm the observation and to establish a new animal model system, hybrids between female Japanese and male Chinese toads were newly generated from 3 pairs of parents and pathological changes in their kidneys were examined sequentially over 6 years.

Iron overload augments angiotensin II-induced cardiac fibrosis and promotes neointima formation.

Background: Abnormal iron deposition may cause oxidant-induced damage in various organs. We have previously reported that continuous administration of angiotensin II to rats results in an overt iron deposition in the renal tubular epithelial cells, which may have a role in angiotensin II-induced renal damage. In the present study, we investigated the role of iron in the development of cardiac injury induced by angiotensin II.

Abnormal iron deposition in renal cells in the rat with chronic angiotensin II administration.

Acute experimental iron loading causes iron to accumulate in the renal tissue. The accumulation of iron may play a role in enhancing oxidant-induced tubular injury by producing increased amounts of reactive oxygen species. From findings in cells from heme oxygenase-1 (HO-1)-deficient mice, HO-1 is postulated to prevent abnormal intracellular iron accumulation.