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Biomedical subjects

F Nishimura

Publications and source records attributed to F Nishimura.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Setting characteristics of calcia-bonded investments by hydration].

Calcium oxide (CaO) slurry mixed with water hardens and expands by hydration. The authors used this setting characteristic as a binder of zirconia-refractory investments. If a mixed slurry was placed in air, unreacted residual calcia powders absorbed water and reverted to calcium hydroxide (Ca (OH)2). This resulted in a large setting expansion that continued for several days. A carbon dioxide (CO2) gas atmosphere controlled this expansion of calcia. When mixed slurry was placed in a carbon dioxide gas atmosphere, calcium carbonate (CaCO3) was formed and prevented the further hydration of unreacted calcium oxide. Thus setting expansion values were controlled. The combined expansion of setting and thermal expansion, in CaO-CO2-bonded zirconia investments, was about 1.5-2.5%. On the whole, calcium oxide is expected to be a good binder for high temperature dental casting refractory.

Calcium↗
PubMed1989

[Fracture toughness of human enamel].

The fracture toughness (KIC) of human enamel was examined by means of Indentation Microfracture Method (IM method). The IM method was a simple, efficient and economical means to obtain KIC of human enamel. Judging from the relationship between load and crack size, a median crack occurred in the range of 2.45-5.88 N, and KIC was hardly affected by the difference of surface roughness. KIC of a 58-year-old man's teeth was 0.61 MPam1/2 in 1 and 0.77 MPam1/2 in 7 and the difference was significant (P less than 0.01). KIC differed much from the direction of the indenter pressed to enamel rods and the KIC of the direction of enamel rods axis I was markedly higher than that of others. In the 58-year-old man's 1, KIC was 0.61 MPam1/2 in the direction of enamel rods axis V, 0.66 MPam1/2 in the direction of H and 0.84 MPam1/2 in the direction of I, and the difference was significant (P less than 0.01). The values for a 10-year-old man's permanent teeth was slightly higher but showed a similar inclination to the 58-yer-old man's teeth.

Dental Enamel↗
PubMed1988

A nasal allergy model developed in the guinea pig by intranasal application of 2,4-toluene diisocyanate.

An experimental model of nasal allergy has been developed in guinea pigs by intranasal application of 2,4-toluene diisocyanate (TDI). A 10% TDI solution in ethyl acetate was painted onto the nasal vestibuli of the animals once a day for 5-10 days. During the course of repeated application of TDI, the number of animals which secreted rhinorrhea containing eosinophils increased. Morphological survey of the nasal mucosa showed infiltration of eosinophils and some other changes indicative of acute inflammation. Moreover, mast cells were found not only in the subepithelial connective tissue but also in the epithelial layer. Nasal mucus obtained from the mucosa has been found to be an effective test material for studies of nasal allergy. A striking decrease of specific granules was found in some mast cells contained in the mucus. In parallel with the symptomatology, biochemical and serological studies suggested the involvement of type I allergy in the experimental system; TDI-specific histamine release from the nasal mucosa and positive passive cutaneous anaphylaxis were found 3 weeks after the application of TDI.

Administration, Intranasal↗
PubMed1987

Contact sensitivity induced in mice by methylene bisphenyl diisocyanate.

An experimental model of contact sensitivity has been developed in C57BL/6 mice using methylene bisphenyl diisocyanate (MDI), a raw material of polyurethane resins. Sensitization through a single epidermal application of 1% MDI solution in ethyl acetate to the backs of the mice resulted in marked ear swelling. The time course of the swelling was characteristic of delayed-type hypersensitivity and the increment of the ear thickness was compatible with that induced by toluene diisocyanate (TDI). Passive transfer of the MDI-induced contact sensitivity was successfully achieved using lymphocytes from the lymph nodes of MDI-sensitized syngeneic mice, and the effector cells were found to be T cells. Cross reaction between MDI and TDI has shown that MDI is not only a potent contact sensitizer but also can form a contact sensitizer group together with TDI.

Administration, Cutaneous↗
PubMed1983

The J wave in accidental hypothermia.

Electrocardiograms of 50 patients with accidental hypothermia were reviewed with regard to the J wave with the following results: (1) J waves were observed in 40 of 50 cases. (2) J waves were recorded most frequently in leads II or V6 (34 of 40 cases, 85%). However, in deep hypothermia, the J wave was often most prominent in leads V3 or V4. (3) The size of the J wave appeared to be related to body temperature. Below 30 degrees C, large J waves were often observed; above 30 degrees C, J waves were usually smaller. (4) J waves were not distinctive in the cases with clockwise rotation. (5) The appearance and the size of the J waves seemed not to be associated with the arterial pH. (6) The J wave decreased in size along with rise of the body temperature. However, a small J wave persisted in many cases even after normothermia was restored. It was also difficult to distinguish these small J waves from small notches at the QRS-ST junction which are sometimes observed in normal individuals not subjected to hypothermia.

Adult↗
PubMed1983

Painless myocardial infarction in diabetics.

In order to evaluate differences between the initial manifestations of acute myocardial infarction (AMI) in diabetics (DM) and non-diabetics (N-DM), 94 consecutive AMIs (DM 40, N-DM 54) were studied over a four-year period. Cases with abrupt onset associated with chest pain and/or discomfort in the areas of the chest and back were classified as the typical group (I). All other cases were classified as the atypical group (II). In subjects over the age of 60, 12 out of 33 DM had atypical manifestations, but only 3 out of 29 N-DM (p less than 0.05). In subjects aged 59 or less, the incidence of atypical cases was similar in the DM and N-DM groups. The initial symptoms of AMI were not correlated with type or location of infarction, nor with the type of treatment or presence of the ankle jerk reflex. Pre-infarction symptoms were present in 69% of Group I and 74% of Group II DM subjects. In Group II, 5 out of 16 patients had a history of typical angina, but had no chest pain at the onset of infarction. The post-AMI mortality within one month was 15% in the DM and 18% in the N-DM group. It was 14% in Group I and 25% in Group II. Mean CPK did not differ statistically between Group I and Group II. However, the Peel prognostic index was 11.0 +/- 5.1 for Group I and 15.5 +/- 5.0 for Group II (p less than 0.05) in subjects over the age of 60.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Choroidal neovascularization in long-standing case of Vogt-Koyanagi-Harada disease.

The eyes in a case of Vogt-Koyanagi-Harada disease (VKH) with long-standing uveitis for 26 years after the onset were studied histopathologically. It was found that typical granulomatous inflammation was persistent in the uveal tract and the choroidal neovascularization occurred in the peripheral fundus accompanied by proliferation of the retinal pigment epithelial cells (RPE). Some of the new vessels under the pigment epithelium extended into the vitreous. It was concluded that the ocular inflammation of VKH was essentially granulomatous even in this long-standing case. Disappearance of choroidal melanocytes, existence of epithelioid cells containing pigment granules, and accumulation of lymphocytes and plasma cells in the lesion indicated that the inflammation was an autoimmune reaction against uveal melanocytes, although the trigger initiating the disease remains unknown. It was further concluded that the peripheral fundus as well as the peripapillary and macular areas was a predilected site for choroidal neovascularization in chronic uveitis. The choroidal neovascularization may develop in such a way that the uveal inflammation damages the Bruch's membrane and choriocapillaris and consequently causes retinal ischemia, thus stimulating the endothelium of the choriocapillaris and the overlying RPE to proliferate. There is a close relation between choroidal neovascularization and proliferation of RPE. Choroidal neovascularization may cause reactive proliferation of the RPE and vice versa.

Choroid↗