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Biomedical subjects

F Nishimura

Publications and source records attributed to F Nishimura.

At least 55 records · Page 3Linked to original sources
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↗