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Biomedical subjects

S Usami

Publications and source records attributed to S Usami.

At least 217 records · Page 12Linked to original sources
PubMed1970

Abnormal rheology of oxygenated blood in sickle cell anemia.

The viscosity of oxygenated blood from patients with sickle cell anemia (Hb SS disease) was found to be abnormally increased, a property which contrasts with the well recognized viscous aberration produced by deoxygenation of Hb SS blood. Experiments designed to explain this finding led to considerations of deformation and aggregation, primary determinants of the rheologic behavior of erythrocytes as they traverse the microcirculation. Deformability of erythrocytes is in turn dependent upon internal viscosity (i.e. the state and concentration of hemoglobin in solution) and membrane flexibility. Definition of the contribution made by each of these properties to the abnormal viscosity of oxygenated Hb SS blood was made possible by analysis of viscosity measurements, made over a wide range of shear rates and cell concentrations, on Hb SS erythrocytes and normal erythrocytes suspended in Ringer's solution (where aggregation does not occur) and in plasma. Similar measurements were made on the two cell types separated by ultracentrifugation of Hb SS erythrocytes: high density erythrocytes composed of 50 to 70% irreversibly "sickled" cells (ISC) and low density erythrocytes composed of over 95% non-ISC. Under all experimental conditions (hematocrit, shear rate, and suspending medium) the viscosity of ISC exceeds that of normal erythrocytes. The viscosity of non-ISC is elevated only in the absence of aggregation and over intermediate ranges of hematocrit. Analyses of the data reveal (a) an elevated internal viscosity of ISC: (b) a reduced membrane flexibility of both ISC and non-ISC, particularly at low shear rates; and (c) a reduced tendency for aggregation displayed by both cell types. The abnormal viscosity of oxygenated Hb SS blood can be attributed to the altered rheology of ISC and, to a lesser extent, of non-ISC. These studies assign a role to the abnormal rheology of Hb SS erythrocytes in the pathogenesis of sickle cell anemia, even under conditions of complete oxygenation.

Adolescent↗
PubMedDate not supplied

Development of a side-view chamber for studying cell-surface adhesion under flow conditions.

Observing microscopic specimens is often useful in studies of cellular interaction with a vascular wall. We have developed an in vitro side-view flow chamber that permits observations from the side of the cell's contact with various adhesive surfaces under dynamic flow conditions. This side-view flow chamber consists of two precision rectangular glass tubes called microslides. A smaller microslide is inserted into a larger one to create a flow channel with a flat surface on which either cultured vascular endothelium can be grown or purified adhesion molecules can be coated. Two optical prisms with a 45 degrees chromium-coated surface are used along the flow channel to generate light illumination and observation pathways. The side-view images of cell-substrate contact can be obtained using a light microscope. This design allows us not only to measure the effects of flow on cell-surface adhesion strength, but also to have close observation of cell deformation and adhesive contact to various surfaces in shear flow. In addition, this chamber can readily serve for a conventional top-view flow channel, similar to the parallel-plate flow chambers used in many areas. The development of such a side-view flow chamber can be beneficial to various in vitro applications in cellular studies that require an edge view, especially for various cell interactions with cultured vascular endothelium or surfaces containing single-type adhesive molecules under flow conditions.

Animals↗
PubMedDate not supplied

Sensorineural hearing loss caused by mitochondrial DNA mutations: special reference to the A1555G mutation.

Mutations in mitochondrial DNA, which are maternally inherited, have been thought to be one of the causes of sensorineural hearing loss. Two mitochondrial mutational sites (A1555G, A7445G) have been reported to be responsible for non-syndromic hearing impairments. The A1555G mutation causes increased susceptibility to aminoglycoside antibiotic-induced hearing loss as well as non-syndromic sensorineural hearing loss. Our wide screening study showed that there may be a great number of subjects within the Japanese population who have the A1555G mutation. Recent reports suggest that high-risk populations may exist throughout the world. The aminoglycoside-induced hearing loss associated with a mitochondrial mutation is commonly bilateral, symmetric, high frequency involved, and is sometimes associated with progressive sensorineural hearing loss.

Adult↗