A case of episodic angioedema associated with blood eosinophilia: upregulated C5a receptor expression on eosinophils.

A 47-year-old woman was admitted to hospital complaining of swelling and pain of the extremities, accompanied by high fever and generalized erythema. Laboratory examination showed marked blood eosinophilia with elevation of IgM, IgE, and C-reactive protein. All autoantibodies examined were negative. The heart and lungs showed no untoward findings. Biopsies of the skin and muscle revealed cellular infiltration of eosinophils around small blood vessels. Quantitation of C5a receptor (C5aR) expression by flow cytometry using anti-C5aR antibody showed upregulated expression of C5aR on blood eosinophils but downregulated expression on neutrophils. The abnormal C5aR expression on eosinophils and neutrophils became normal after spontaneous resolution of symptoms and blood eosinophilia. The possibility that C5aR expression on granulocytes is related to the pathogenesis of this syndrome may be considered.

Macrophage recognition of saccharide chains on the erythrocytes damaged by iron-catalyzed oxidation.

Mouse erythrocytes oxidized with an iron catalyst ADP/Fe3+ chelate attached to the monolayers of mouse resident and thioglycollate-induced peritoneal macrophages in the absence of serum, indicating that the macrophages recognized the oxidized erythrocytes. The recognition was partially prevented when the oxidized cells were treated with dithiothreitol, suggesting that disulfide formation is involved, in part, in the generation of the membrane sites recognized by macrophages. Phosphatidylserine is unlikely to be the determinant on the oxidized cells because it was not detected on the outer surface of the oxidized cells. The recognition by resident macrophages was effectively inhibited by N-acetylneuramin lactose, N-acetylneuraminic acid, glycophorin A, and disialoganglioside GD1a, but poorly by lactose, asialoglycophorin A, and monosialoganglioside GM1. In addition, the recognition was partially inhibited by L-fucose and human lactoferrin. The recognition by thioglycollate-induced macrophages was not inhibited by glycophorin A but was partially inhibited by L-fucose, lactoferrin, and oligosaccharides from band 3 glycoprotein. Enzymatic cleavage of the poly-N-acetyllactosaminyl saccharide chains of band 3 and lactoferrin resulted in a loss of the inhibitory activity. These results suggest that sialosaccharide chains of ADP/Fe(3+)-oxidized erythrocytes, possibly those on glycophorin A, are mainly involved in the recognition by resident macrophages, and poly-N-acetyllactosaminyl saccharide chains, possibly those on band 3, are partly involved in the recognition both by resident and thioglycollate-induced macrophages. Oxidation of erythrocytes may induce change in these membrane glycoproteins, like aggregation, which renders their saccharide chains susceptible to the macrophage recognition.

[Analysis by two-dimensional electrophoresis of the cause of myocardial dysfunction in aging rat hearts].

The severity and frequency of atherosclerosis, diabetes, and ischemic heart disease, which affect cardiac function, increase with aging. Although there are many reports about hemodynamic and histopathological studies about aging hearts, there are very few studies on changes in structural proteins in aging hearts. We investigated the contractile proteins of the left ventricles in rats aged 6, 12 and 125 weeks using two-dimensional electrophoresis. There were no difference in structural proteins in heart between 6-week and 12-week-old rats. The contents of myosin heavy chain, myosin light chain 2, actin, troponin-I in 125-week-old rats decreased compared with those of 12-week-old rats. Myosin heavy chain, which is one component of myosin, interacts with actin and changes chemical energy to mechanical energy. Therefore its decrease leads to a decline in myocardial contractility. These results seem to indicate one of the most important changes in the aging rat heart, as well as impairment in relaxation by the increase of interstitial fibrosis and decline of Ca uptake by sarcoplasmic reticulum.

[Radiological changes in the femoral side after cementless total hip arthroplasty].

We investigated radiological and functional changes of the femurs with cementless total hip arthroplasty. Our particular attention was paid to the relationship between the thigh pain and the rate, period of its incidence and the progression of radiological changes. The cases studied consisted of 57 female patients with severe coxarthrosis who were implanted with a SUS316-L macroanchoring type of THP (JIAT). Clinical evaluations, radiographic findings in the femoral side, and osteometric observations were carried out periodically in the period before surgery until five years after surgery. The JOA criterion at the time of the final examination was average 91 points. However, we observed a high degree of bone change in the femur on the radiogram. Of 63 hips, there was 71% cortical bone atrophy, a 43% reduction of cortex thickness, 25% cortical bone hypertrophy, 94% endosteal bone bridging in the stem tip, a 64% linear sclerosis of the neighboring stem, and a 37% enlargement of the medullary cavity. Bone atrophy was manifested soon after surgery, and there was 34% recovery. Further, there was no connection between thigh pain and bone changes. We, therefore, concluded that such bone changes as atrophy would not immediately bring about adverse consequences.

[A case of Swyer-James syndrome diagnosed by selective alveolobronchography].

A 33-year-old male was admitted to our hospital for further investigation of unilateral hyperlucency of the left upper and middle lung fields on chest X-ray. A pulmonary scan showed decreased perfusion of the left upper and middle lung fields. Pulmonary arteriography demonstrated small left pulmonary arteries with diminished peripheral vascular branches. Left bronchogram showed almost normal distribution of main and subsegmental bronchi, but poor filling by contrast in the peripheral bronchi. From these findings, the patient was diagnosed as having Swyer-James syndrome. In order to demonstrate the alveoli in this syndrome, selective alveolobronchography (SAB) was performed. SAB revealed coarse ring shadows of B1+2.

Somatosensory and acoustic brain stem reflex myoclonus.

A patient with brain stem reflex myoclonus due to a massive midbrain infarct was studied electrophysiologically. Myoclonic jerks were elicited at variable latencies by tapping anywhere on the body or by acoustic stimuli, and mainly involved flexor muscles of upper extremities. The existence of convergence of somatosensory and acoustic inputs in the brain stem was suggested. This myoclonus seemed to be mediated by a mechanism similar to the spino-bulbo-spinal reflex.