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N Iwasa

Publications and source records attributed to N Iwasa.

7 recordsLinked to original sources
PubMed2003

Coulomb dissociation of 8B and the low-energy cross section of the 7Be(p,gamma)8B solar fusion reaction.

An exclusive measurement of the Coulomb breakup of 8B into 7Be+p at 254A MeV allowed the study of the angular correlations of the breakup particles. These correlations demonstrate clearly that E1 multipolarity dominates and that E2 multipolarity can be neglected. By using a simple single-particle model for 8B and treating the breakup in first-order perturbation theory, we extract a zero-energy S factor of S17(0)=18.6+/-1.2+/-1.0 eV b, where the first error is experimental and the second one reflects the theoretical uncertainty in the extrapolation.

Journal Article↗
PubMed2002

Momentum distribution of 15B fragments from the breakup of 17B.

The two-neutron removal cross section (sigma(-2n)) and the longitudinal momentum distribution of 15B fragments from the breakup of 17B on 9Be were measured at 70A MeV. The distribution in the projectile rest frame is characterized by a FWHM of 80+/-10 MeV/c for 15B. The sigma(-2n) is found to be 0.22+/-0.05 b. A Glauber-type analysis of the data provides clear evidence of a two-neutron halo structure in 17B.

Journal Article↗
PubMed2001

Photoneutron cross sections for unstable neutron-rich oxygen isotopes.

The dipole response of stable and unstable neutron-rich oxygen nuclei of masses A = 17 to A = 22 has been investigated experimentally utilizing electromagnetic excitation in heavy-ion collisions at beam energies about 600 MeV/nucleon. A kinematically complete measurement of the neutron decay channel in inelastic scattering of the secondary beam projectiles from a Pb target was performed. Differential electromagnetic excitation cross sections d sigma/dE were derived up to 30 MeV excitation energy. In contrast to stable nuclei, the deduced dipole strength distribution appears to be strongly fragmented and systematically exhibits a considerable fraction of low-lying strength.

Journal Article↗
PubMed1999

Recurrence factors for chronic subdural hematomas after burr-hole craniostomy and closed system drainage.

Recurrence of chronic subdural hematoma after burr-hole craniostomy and closed system drainage is not uncommon. We sought to identify risk factors for recurrence. In 121 patients, various factors including age, initial neurologic status, hematoma thickness, computed tomographic density of the hematoma, midline shift, multiplicity, systemic disease, and drainage volume were compared retrospectively between nonrecurring cases and recurring cases. Recurrence was noted in 10 cases (8.3%). In recurring cases, the drainage volume was significantly larger than in nonrecurring cases, and the recurrence rate increased in proportion to drainage volume. Other factors significantly influencing recurrence were hematoma thickness and associated diabetes mellitus. Drainage contents mainly derived from either exudate within the subdural membrane or cerebrospinal fluid leakage. Entry of cerebrospinal fluid into the hematoma cavity or continuing leakage of serum components through opened endothelial gap junctions are considered to be major causes of increased drainage volume, leading in turn to recurrence of the hematoma.

Adult↗
PubMed1997

Hypothalamic pilocytic astrocytoma presenting with intratumoral and subarachnoid hemorrhage.

A 45-year-old male presented with sudden onset of severe headache. Computed tomography and magnetic resonance imaging demonstrated an irregularly enhanced suprasellar mass with intratumoral and subarachnoid hemorrhage. The mass was removed in two operations. Histological examination of the tumor revealed pilocytic astrocytoma. The relatively rich vascularity and perivascular tumor cell proliferation observed in this benign lesion were probably the causes of this extremely rare association.

Astrocytoma↗
PubMed1975

Two autopsy cases of diffuse gastrointestinal polyposis with ectodermal changes. Cronkhite-Canada syndrome.

Two autopsy cases of Cronkhite-Canada syndrome were reported. The caused of hypoproteinemia, electrolyte imbalance and ectodermal changes were discussed with reference to previously reported cases. The mechanism of protein loss was probably due to outflow into the intestinal lumen of the mucous substance in the cystically dilated glands, directly and/or indirectly followed by loss of mucosal surface. Electrolyte imbalance probably developed from gastrointestinal loss as well as poor substitution. The ectodermal changes were probably not a subsequent part of the emaciation or hypoproteinemis, but an inherent part of this disease. Therapy, whether substitution or surgical procedure, should be selected in order to control the general condition of the patient.

Adult↗