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Biomedical subjects

T Horio

Publications and source records attributed to T Horio.

At least 235 records · Page 13Linked to original sources

Ultraviolet-B radiation suppresses mast cell degranulation induced by compound 48/80.

This study was designed to investigate the effect of middle-wave ultraviolet (UVB) radiation on mast cell functions using mouse ear skin as an in vivo model. Groups of UVB-irradiated BALB/c mice were given an intradermal injection of the mast cell degranulator compound 48/80 into ears at various time intervals (30 min-7 days) after a single exposure to a bank of fluorescent sunlamp tubes (10-100 mJ/cm2). Both the compound-evoked ear swelling response (ESR) and mast cell degranulation were significantly suppressed by preexposure to UVB (25-100 mJ/cm2) after 0 (30 min) to 3 days postirradiation, with a subsequent recovery by day 7. No such effects were observed in mice irradiated with 10 mJ/cm2. The ESR induced by 5-hydroxytryptamine was not significantly affected by UVB radiation during the experimental period. While within this dose range UV radiation itself caused neither loss of mast cell counts nor a measurable degree of degranulation in ear skin, exposure to larger amounts of UV energy (200-500 mJ/cm2) produced tremendous ear swelling with histologic features of mast cell degranulation in an early phase of inflammation. The results suggest that UVB radiation exerts a dual effect on mast cells and that administration of smaller amounts of UVB may alter the mast cell/vasoactive amine system, suppressing ear swelling in response to the degranulator. Vascular reactivities to vasoactive amines were not affected by UVB irradiation.

Animals↗

Effect of 8-methoxypsoralen plus long-wave ultraviolet (PUVA) radiation on mast cells. II. In vitro PUVA inhibits degranulation of rat peritoneal mast cells induced by compound 48/80.

Rat peritoneal mast cells incubated with a histamine liberator, compound 48/80, showed a significantly reduced capacity for releasing histamine following in vitro treatment with 0.1 micrograms/ml of 8-methoxypsoralen (8-MOP) plus 1-5 J/cm2 of long-wave ultraviolet (UVA) irradiation (PUVA). No remarkable inhibition in histamine release was observed in the cells treated with 8-MOP only. Irradiation with 5 J/cm2 of UVA alone exerted an inhibitory effect on histamine release, to a lesser extent than PUVA. PUVA irradiation did not bring any decrease in cell viability or any spontaneous release of histamine from irradiated cells as shown by phase-contrast microscopy and by histamine assay, respectively. These results suggest that PUVA treatment may cause a noncytotoxic disturbance at mast cell membranes or on surface receptors, leading to a decreased capacity for secreting chemical mediators.

Animals↗

Persistent light reaction: induction in the guinea pig.

Persistent light reactions similar to those in humans were observed in the study of photoallergenicity of chemicals in guinea pigs. The animals photoinduced with chemicals reacted to long-wavelength ultraviolet (UVA) radiation in the absence of test materials at the challenge stage. The sensitivity of the animals to UVA persisted for more than 1 year. The minimum erythema dose to UVB of animals in the treated group was less than that in the control group. Our investigations indicate that the main factors influencing the elicitation of persistent light reaction were the amount of Freund's complete adjuvant (FCA) used to enhance the allergic response in animals, and the UVA dose at the induction stage. Based on these findings, we have developed a method to make animals persistent light reactors with high frequency. This method consists of 1 intradermal injection of 1.2 ml emulsified FCA, 5 irradiations with 20.4 J/cm2 of UVA, and topical applications of 5% p-aminoethylbenzoate (benzocaine) at the induction stage. We also found that photosensitivity could be induced using FCA and UVA without photosensitizers.

4-Aminobenzoic Acid↗

Lichen striatus.

The possible relationship between lichen striatus and atopy was studied. Twenty-six patients with typical lichen striatus were studied, and 22 (84.6%) had a positive history of atopic disorders. This might indicate that the pathogenesis of lichen striatus has a close relationship to that of atopic disorders.

Adolescent↗

Prurigo pigmentosa: a possible mechanism of action of sulfonamides.

The patient described here had all the clinical features (itchy red papules and reticular pigmentation) as well as the histological findings (lichenoid tissue reactions) of prurigo pigmentosa, a little-known disorder of unknown etiology, and responded well to sulfamethoxazole treatment. In order to investigate the mode of action of this drug and thus the underlying pathogenesis of this dermatosis, the effect of sulfamethoxazole on the production of oxygen intermediates (OIs) was examined both in the cell-mediated system and in the xanthine-xanthine oxidase system. It was found that therapeutic doses of the drug significantly reduced the hydroxyl radical levels, one of the most potent oxidants that might cause tissue injury. These findings suggest the possibility that OIs produced by infiltrated cells are involved in the inflammatory process of prurigo pigmentosa and that sulfonamides exert their anti-inflammatory effects by affecting OI generation which results in protection against lichenoid tissue reaction.

Administration, Oral↗

PUVA irradiation restores altered binding patterns of lectins in psoriatic epidermis.

We examined a series of biopsy specimens obtained from lesional skin in five psoriatic patients receiving topical PUVA treatment to see the effect of PUVA on epidermal cell membrane glycoconjugates by fluorescent staining techniques using lectins as surface markers. In psoriatic epidermis, Ulex europaeus agglutinin and Concanavalin A depicted only cytoplasmic patterns and did not show the plasma membrane fluorescence that was normally seen in nonpsoriatic skin. Following PUVA treatment, these altered staining patterns gradually normalized, with the appearance of the plasma membrane fluorescence. Restoration of the membrane staining tended to precede improvement in clinical and histologic features of psoriasis, suggesting that normalization of the altered profiles of membrane glycoconjugates is one of the beneficial effects of PUVA irradiation on psoriatic epidermis.

Adult↗

Dense distribution of nuclear alkaline protease to nucleoli with increase in rapidly growing cells in rats.

Neutral and alkaline proteases (chymotrypsin-like serine proteases) are tightly bound to chromatin in nuclei of various tissues of rats, and rapidly growing cells are abundant in the latter enzyme. Activities per mg DNA of these enzymes were measured with fractions of euchromatin, heterochromatin, nucleoli and extranucleoli from normal and regenerating livers, and Rhodamine sarcoma. With normal liver, both enzymes, respectively, were almost evenly distributed among the fractions, except that alkaline protease was significantly higher in nucleoli. The nucleolar alkaline protease increased by 30-60% with regenerating liver and by higher than 100% with the tumor.

Animals↗

Characterization of a growth-inhibiting protein present in rat serum that exerts a differential effect on in vitro growth of nonmalignant rat liver cells when compared with Rous sarcoma virus-transformed rat liver cells.

We have previously reported the transformation by Rous sarcoma virus of a cloned epithelial cell line (BRL) established from Buffalo rat liver by H. Coon. The nontransformed (BRL) and transformed (RSV-BRL) cells grew at comparable rates in culture, whereas only the transformed cells were tumorigenic in vivo. We report here on the existence in rat and mouse sera of a growth inhibitor for the nontransformed BRL cells. The transformed BRL cells (RSV-BRL) were insensitive to this inhibitor. The inhibitory activity was not prominent in sera from other species of animals tested except for rabbit; this serum inhibited the growth of RSV-BRL cells more strongly than that of BRL cells. The growth inhibitor was partially purified from rat serum. It is a protein free of lipid and has a molecular weight of about 220 000. The inhibitor could be separated into three components of pI 4.6, 5.2 (major) and 5.6 by isoelectric electrophoresis.

Animals↗

Isolation, characterization, and comparison of a ubiquitous pigment-protein complex consisting of a reaction center and light-harvesting bacteriochlorophyll proteins present in purple photosynthetic bacteria.

Protein complexes (photochemical reaction complex; PR complex) bound to both light-harvesting bacteriochlorophyll-1 (LH-Bchl-1) and reaction center Bchl (RC-Bchl) were purified from Rhodospirillum rubrum (wild and carotenoid-less), Rhodopseudomonas sphaeroides (wild), and Chromatium vinosum (wild). Another protein complex (LH-2 complex) bound to LH-Bchl-2 was also purified from Rps. sphaeroides. The bacteria were grown in the presence of a [14C]amino acid mixture. The purification procedure included molecular-sieve chromatography in the presence of cholate-deoxycholate, and non-equilibrated isoelectric electrophoresis with 3-[(3-cholamidopropyl)dimethylamino]-1-propanesulfonate. The purified complexes were separated into their constituent proteins by sodium dodecylsulfate-polyacrylamide gel electrophoresis. The molar ratios of the proteins were determined by comparing their radioactivities divided by their molecular weights after consideration of the molecular masses of the complexes. The PR complexes all contained per mol: 1 mol each of RC H-, M-, and L-subunits, 10-13 (probably 12) mol each of two other proteins with molecular weights of 11-12K and 8-11K, 28-32 mol Bchl, 13-15 mol carotenoids (except in the carotenoid-less mutant), 2.6-3.9 mol ubiquinone (or menaquinone in Chr. vinosum), and 53-79 mol phosphate without phospholipid. The LH-2 complex contained per mol: 1 mol 52K protein, about 13 (probably 12) mol each of 9K and 8K proteins, 30 mol Bchl, 10 mol carotenoids, and 38 mol phosphate without phospholipid. The PR complexes and LH-2 complex showed similar X-ray diffraction patterns, implying that they had similar, highly organized molecular structures.

Bacterial Proteins↗

Alteration of lymphocyte functions by 8-methoxypsoralen and longwave ultraviolet radiation. I. Suppressive effects of PUVA on T-lymphocyte migration in vitro.

We investigated the influence of 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet radiation (PUVA) on lymphocyte migration in vitro. Nylon wool-purified, mouse splenic T lymphocytes showed locomotive responses to casein, normal mouse serum (NMS), and zymosan-activated mouse serum (ZAS). Migratory responses to casein and NMS, and to ZAS were remarkably suppressed in lymphocytes exposed to 0.5 J/cm2 UVA plus 0.1 micrograms/ml 8-MOP and to 0.8 J/cm2 UVA plus 8-MOP, respectively. The PUVA treatment used in the present study had no effect on random movement and lymphocyte viability. T lymphocytes cultured in the absence of mitogenic agent for 24 h demonstrated a greater increase in their migration activity than noncultured cells, while lymphocytes cultured after 1.0 J/cm2 PUVA pretreatment remained low. These findings suggest that the therapeutic effect of PUVA on inflammatory skin disorders may be due in part to the suppression of lymphocyte migration.

Animals↗

Effect of ultraviolet irradiation on mast cell-deficient W/Wv mice.

The effect of UV irradiation on the skin was investigated in (WB-W/+) X (C57BL/6J-Wv/+)F1-W/Wv mice, which are genetically deficient in tissue mast cells. Their congenic littermates (+/+) and normal albino mice (ICR or BALB/c) were used as controls. Mice were irradiated with 500 mJ/cm2 of UVB and the increment of ear thickness was measured before and 6, 12, and 24 h after irradiation. Ear swelling in W/Wv mice at 12 and 24 h after irradiation was significantly smaller than that in +/+ and ICR mice. In contrast, the number of sunburn cells formed 24 h after UVB irradiation (200 or 500 mJ/cm2) was similar in W/Wv, +/+ and ICR mice. On the other hand, when mice were treated with 8-methoxy-psoralen (0.5%) plus UVA irradiation (4 J/cm2) (topical PUVA), ears of W/Wv and BALB/c mice, which were both white in color, were thickened similarly 72 h after treatment, but less swelling was observed in +/+ mice, which were black in skin color. The amount of prostaglandin D2 (PGD2) in ears, determined by radioimmunoassay specific for PGD2, was elevated 3-fold in +/+ and ICR mice at 3 h after irradiation with 500 mJ/cm2 of UVB in comparison with basal level without irradiation. However, such elevation was not observed in W/Wv mice. These results suggest that mast cells play an important role in UVB-induced inflammation, and PGs from mast cells are responsible at least in part for the development of this reaction. However, neither mast cells nor PGs contribute to the sunburn cell formation and ear swelling response by PUVA treatment.

Animals↗

The effect of 8-methoxypsoralen plus long-wave ultraviolet (PUVA) radiation on mast cells: PUVA suppresses degranulation of mouse skin mast cells induced by compound 48/80 or concanavalin A.

In order to see whether 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet (UVA) radiation (PUVA) has an influence on immediate-type skin reactions, we have undertaken an animal study. Ears of mice were treated with a 0.5% 8-MOP solution topically plus UVA radiation (1.5-2.5 J/cm2). After PUVA radiation, skin responses to intradermal injection with mast cell liberators, including compound 48/80 (2.5 mg/ml, 10 microliter) and concanavalin A (Con-A) (2.0 mg/ml), or with a mixture of 5-hydroxytryptamine (5-HT) and histamine as vasodilator (1.0 mg/ml and 50 mM, respectively) were examined with time (2 h-14 days). At each time point, an ear swelling response (ESR) was measured with a dial thickness gauge. The rate of mast cell degranulation and mast cell numbers were assessed by light microscopy using toluidine blue-stained semithin (1 micron) sections. ESR induced by compound 48/80 or Con-A was significantly suppressed dose-dependently (greater than 42% inhibition) by PUVA between 2 h-3 days postirradiation as compared with that in nonirradiated control mice, and the value returned to normal levels by 7-14 days. Compound 48/80- or Con-A-induced mast cell degranulation (%) was remarkably decreased between 2 h-3 days (greater than 48% inhibition) in accordance with the suppression in ESR and it was restored to the rates in nonirradiated controls by 7-14 days. Neither ESR nor percent degranulation was affected by UVA radiation only (less than 3.5 J/cm2) or application of 8-MOP only. 5-HT plus histamine-mediated ESR was not altered at all by PUVA throughout the experimental period. Since PUVA radiation itself at given doses did not produce measurable ESR, mast cell degranulation, or a reduction in mast cell numbers, and since PUVA did not affect a normal vascular response to vasodilator, it seemed that decreased skin reactivity to mast cell degranulators by PUVA might be due to a PUVA-induced noncytolytic alteration in mast cell release mechanisms.

5-Hydroxytryptophan↗

In vitro PUVA radiation abolishes fluorescent staining with epidermal cell and basement membrane zone markers.

The purpose of this study was to investigate whether 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet (UV-A) light irradiation (PUVA) had a direct effect on the expression of epidermal cell and basement membrane zone (BMZ) markers without altering intracellular metabolic pathways. Cryostat sections of guinea-pig skin were covered with an 8-MOP solution and irradiated in vitro with UV-A light. Treated sections were stained subsequently with various membrane markers including pemphigus sera, pemphigoid sera (BMZ marker) and a group of biotin-labelled lectins (Concanavalin-A, peanut agglutinin, soybean agglutinin, Ulex europeus agglutinin (UEA) and wheat germ agglutinin). Fluorescent staining with all reagents except for UEA was reduced appreciably in intensity by PUVA radiation at higher energy doses (20 micrograms/ml of 8-MOP plus 20-30 J/cm2 of UV-A). Radiation with lower energy doses did not affect membrane marker staining. Weakened or abolished marker staining was restored to normal when scavengers of oxygen intermediates such as superoxide dismutase (540-5400 units/ml) or sodium azide (10-200 mM) were added to the 8-MOP solution during UV-A irradiation. UEA staining was negative in both PUVA-irradiated and untreated guinea-pig skin. PUVA at higher energy doses appeared to cause tissue damage by photodynamic reactions, resulting in decrease in membrane marker staining.

Animals↗

Micropapular sarcoidosis simulating lichen nitidus.

A 28-year-old woman with sarcoidosis had military, skin-colored papules localized on the upper back. The lesions closely simulated lichen nitidus. Histologic examination of the papule demonstrated the naked granuloma encircled by epidermal collarettes in the papillary dermis. Therefore, the microscopic reaction pattern also resembled those of lichen nitidus. This case is a unique form of micropapular sarcoidosis in respect to the clinical appearance and microscopic changes.

Adult↗