Kenichi Uyeno

Reticulate hyperpigmentation distributed in a zosteriform fashion: a new clinical type of hyperpigmentation

We have recently seen two cases of hyperpigmentation in children, which was reticulate and distributed in a zosteriform fashion. As another two cases of hyperpigmentation of this kind in children have been reported previously, described as reticulate hyperpigmentation distributed in a zosteriform fashion,1,2 this gives a total of four cases of hyperpigmentation of this kind reported recently from Japan.

Chromomycosis. A case with a widespread rash, lymph node metastasis and multiple subcutaneous nodules

Summary:  The patient is a male aged 62 living in Ibaraki Prefecture. Eight years ago, a rash first appeard on the left side of the lower back during summer. Two years later, the rash had spread to almost the entire body. In 1983, he was diagnosed by the dermatological department of the Mito Kyodo Hospital as having chromomycosis due to Fonsecaea pedrosoi. He received treatment using flucytosine without any significant improvement. Superficial lymph node swellings and multiple subcutaneous nodules appeared in December of 1985. He entered our institute in May of 1987.

Proton radiotherapy of skin carcinomas

Summary At the Proton Medical Research Center, University of Tsukuba, we performed a pilot study of protonbeam radiotherapy in 12 patients with the following types of carcinoma: Bowens disease (4), oral verrucous carcinoma (5), and squamous cell carcinoma (3). They received total doses of 51–99.2 Gy in fractions of 2–12.5 Gy. All of the tumours responded well to the treatment. All four lesions of Bowens disease, three of the five oral verrucous carcinomas, and the three squamous cell carcinomas completely regressed following irradiation. Two squamous cell carcinomas recurred during the followup period. One recurrent squamous cell carcinoma was successfully treated by a salvage surgical operation, and in the other case the patient refused further therapy. In two verrucous carcinomas there was 90% regression of tumour volume. No severe radiation‐related complication occurred. As proton radiotherapy produces good local tumour control without significant morbidity to the surrounding normal tissues, it may prove to be a useful therapeutic modality for the treatment of skin carcinomas.

Monocyte activating factor in sarcoidosis. I: Existence of the factor in sarcoidosis sera

Sarcoidosis sera were found to have the ability to induce normal human monocytes to spread. Gel filtration of sarcoidosis sera on Sephadex G-200 showed that the factor mainly responsible for this activity had a molecular weight of about 70,000. The spreading factor also possessed the ability to increase all cell size of normal human monocytes as well as to increase their phagocytosis and glucose consumption. Accordingly, the spreading factor seems to be considered as a monocyte activating factor. Sarcoidosis sera showed a macrophage migration inhibitory activity, as well. On Sephadex G-200 column chromatography of the sera, the most obvious inhibitory activity was eluted in the fraction with a molecular weight of about 45,000. The macrophage migration inhibitory factor had the ability neither to increase cell size of normal human monocytes nor to increase their phagocytosis and glucose consumption.

Effect of Human Fibroblast Interferon on Normal Human Monocyte Activation Induced by a Factor Found in Sarcoidosis Sera

Effect of human fibroblast interferon (IFN‐β) on normal human monocyte activation induced by the monocyte activating factor found in sarcoidosis sera was studied. Spreading was used as one indicator of monocyte activation. IFN‐β was shown to inhibit spreading of normal human monocytes induced by the activating factor. The inhibitory activity of IFN‐β against monocyte spreading was adsorbed with monoclonal antibody to human IFN‐β‐Sepharose beads. Increases in phagocytosis and glucose consumption of normal human monocytes induced by the activating factor was also inhibited by IFN‐β. Recombinant IFN‐β also showed similar inhibitions.

Surface Densities of Murine Ia + Dendritic Epidermal Cells (Ia + DECs) and Thy-1 + Dendritic Epidermal Cells (Thy-1 + DECs) in Relationship to Aging and Ultraviolet B (UVB) Radiation

Identification and enumeration of both Ia + dendritic epidermal cells (Ia + DECs) and Thy‐1 + dendritic epidermal cells (Thy‐1 + DECs) from various parts of the body and non‐irradiated and ultraviolet B (UVB) irradiated back skin were examined using epidermal sheets of C3H/He inbred mice of different age groups and indirect immunofluorescent technique. The following results were obtained: [1] There was a significant decline in both Ia + DEC and Thy‐1 + DEC density in the mice in the oldest group (48–50 weeks); [2] The densities of Ia + DECs were significantly higher than those of Thy‐1 + DECs in comparisons of various parts of the body; [3] At 24 h after 60–120 mJ/cm2 UVB irradiation, the Ia + DECs and Thy‐1 + DECs decreased significantly in a dose‐dependent fashion. The Ia + DECs decreased drastically (p<0.01) while the Thy‐1 + DECs decreased mildly (p<0.05). [4] The degree or resistance to UVB differed between Ia + DECs and Thy‐1 + DECs in older mice (40–48 weeks). These findings may imply that the decline of the Ia + DECs and Thy‐1 + DECs reflects alterations in immune response during aging; As do Ia + DECs, Thy‐1 + DECs might also play a role in UVB induced specific unresponsiveness in contact hypersensitivity; each type of Ia + DECs and Thy‐1 + DECs follows a distinct biological kinetic pattern after UVB irradiation.

Monocyte activating factor in sarcoidosis: II. Secretion of the factor from monocytes

The normal human monocytes pretreated with the monocyte activating factor found in sarcoidosis sera were shown to secrete a factor which induced normal human monocytes to spread as well as to increase their cell size. Phagocytosis and glucose consumption of normal human monocytes were also increased by this secondarily obtained factor. Its molecular weight was about 70,000. These results indicate that this secondary factor may be the same substance as the monocyte activating factor found in sarcoidosis sera. The normal human monocytes pretreated with the monocyte activating factor were also shown to liberate a factor which generated macrophage migration inhibitory factor in cooperation with normal human sera.

Monocyte‐modulating Activities in the Sera of Patients with Granuloma Annulare

Studies were performed to determine whether the sera of the patients with granuloma annulare had monocyte modulating activities. As indicators of monocyte modulation, spreading and aggregation were used. As a control, similar experiments were performed on pooled normal human sera. Normal human monocytes were incubated with either test sera or control sera. The percentage of spread cells was estimated at 6 hr of incubation and that of aggregated cells was estimated at 24 hr of incubation. The percentage of spread cells and aggregated cells in the monocytes incubated with granuloma annulare sera was higher than that of the cells incubated with pooled normal human sera. Thus, granuloma annulare sera may have a greater ability to induce monocytes to spread and aggregate than do normal human sera.

An inhibitory factor against monocyte spreading in the sera of patients with systemic lupus erythematosus.

The effect of the sera of patients with systemic lupus erythematosus (SUE) on monocyte function was studied using cell spreading as an indicator. Monocyte spreading induced by exogenous stimuli was shown to be inhibited by SLE sera. Gel filtration of SLE sera on Sephadex G‐200 revealed that the factor responsible for this inhibition had a molecular weight of about 50,000. Pretreatment of monocytes with the inhibitory factor led to suppression of cell spreading induced by subsequent stimulation, but this hyporeactivity was reversible. Spreading of monocytes was rapidly aborted by the addition of this inhibitory factor. Thus, the inhibitory factor appeared to affect monocyte itself, but its effect seemed to be transient.

A monocyte-aggregating factor in the sera of patients with sarcoidosis.

Sarcoidosis sera were shown to have higher activity in aggregating normal human monocytes than normal human sera. A kinetic study suggested that monocytes may not be sensitive to the aggregating activity of sarcoidosis serum until they develop to some extent into macrophages. Gel filtration of sarcoidosis sera on Sephadex G‐200 showed that the major factor responsible for monocyte aggregation had the molecular weight of about 130,000. This major aggregating factor was unable to increase cell size of normal human monocytes or to increase phagocytosis and glucose consumption of normal human monocytes. It did have the ability to form multinucleate giant cells.