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Biomedical subjects

K Danno

Publications and source records attributed to K Danno.

At least 73 records · Page 4Linked to original sources
PubMed1985

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↗
PubMed1985

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↗
PubMed1984

Alterations in lectin binding to the epidermis following treatment with 8-methoxypsoralen plus long-wave ultraviolet radiation.

The alterations in lectin fluorescence stainings to the epidermis were examined in guinea pig skin treated with topical application of a 1% 8-methoxypsoralen (8-MOP) solution plus long-wave ultraviolet (UVA) radiation (1.5-3.5 J/cm2) (PUVA). Serial biopsy specimens taken up to 21 days postirradiation were stained with 8 commercially available lectins labeled with either fluorescein isothiocyanate (FITC) or biotin (followed by avidin D-FITC): Bandeiraea simplicifolia agglutinin I (BSA), concanavalin A (Con-A), Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA), Ricinus communis agglutinin I (RCA), soybean agglutinin (SBA), Ulex europeus agglutinin I (UEA), and wheat germ agglutinin (WGA). In normal guinea pig skin UEA staining was absent. Following PUVA treatment, UEA and DBA stainings became apparent or stronger in intensity after days 7-14 (UEA) and days 4-7 (DBA), respectively, and returned to negative or weak by days 14-21. Stainings with Con-A, SBA, and WGA gave remarkable decreases in intensity after days 2-4 and recovered to the baseline by days 7-14. Intensity of BSA, PNA, and RCA stainings was decreased to a lesser degree than the other lectins. Such changes were not produced by application of 8-MOP, UVA radiation (less than 10 J/cm2), UVB radiation (900-2700 mJ/cm2), or tape stripping. These results suggest that PUVA treatment perturbs the composition or organization of epidermal cell surface glycoconjugates to induce alterations in lectin stainings.

Animals↗
PubMed1984

Role of oxygen intermediates in UV-induced epidermal cell injury.

To investigate the role of oxygen intermediates (OIs) in sunburn cell (SC) formation and development of UV-inflammation in vivo, groups of mice were injected intravenously with OI scavengers, including bovine blood superoxide dismutase (SOD), bovine liver catalase, L-histidine, D-mannitol, and saline (controls) before and/or after UV irradiation with sunlamp tubes (mainly 280-320 nm; 300 mJ/cm2; UVR). Ear thickness was measured before and 6 and 24 h after UVR. Ears were removed 24 h after UVR and the number of SCs per unit length of ear epidermis was counted using hematoxylineosin stained sections. The number of SCs was significantly decreased (p less than 0.02) by a single injection of SOD (10-30 units/g body weight) given either just before or immediately after (less than 15 min) UVR, while SC formation was no longer suppressed by injections given more than 2 h before or after UVR. Four repeated injections of SOD (10 units/g) also reduced SC counts but did not significantly alter ear-swelling responses (ESR). Neither SC counts nor ESR were remarkably suppressed by 4 injections of any of the other active OI scavengers, inactivated SOD, or bovine serum albumin. A single injection of diethyldithiocarbamate, an SOD inactivator, significantly augmented SC formation (p less than 0.05), but did not change ESR. These findings suggest that OIs generated by UVR participate in SC formation but are not apparently involved in UV-edema.

Animals↗
PubMed1984

Bullous pemphigoid-like lesions induced by phenacetin. Report of a case and an immunopathologic study.

An 84-year-old man with chronic eczema and ischemic heart disease had bullous pemphigoid-like lesions develop following the oral administration of phenacetin. The diagnosis was confirmed by routine histopathologic studies and by immunofluorescent and electron microscopy. Since rechallenge with phenacetin resulted in bulla formation, phenacetin was considered to be the causative agent. This patient showed several atypical clinical features, compared with patients with idiopathic bullous pemphigoid, including no associated erythematous macules, a positive Nikolsky's sign, painful superficial ulcers, and nonpruritic bullae. Histopathologically, there was lack of polymorphonuclear leukocyte infiltrate. The immunopathologic characteristics, however, were quite typical for those found in bullous pemphigoid. The antigenic sites for the autoantibodies from our patient were, at least in part, different from those of idiopathic bullous pemphigoid.

Administration, Oral↗
PubMed1983

Distribution and mobility of concanavalin A receptors on isolated guinea pig epidermal cells at various stages of differentiation.

Trypsinized guinea pig epidermal cells were separated by velocity sedimentation at unit gravity. Based on the relationship between cell size and both morphological and functional aspects of differentiation, the cells were classified as lower (a diameter less than 12.5 micron), middle (a diameter between 12.5 and 15 micron), and upper (a diameter greater than 15 micron) epidermal cells. Fresh cells exposed to rhodaminated concanavalin A (Con A) were sedimented and reacted with fluoresceinated anti-Con A serum to distinguish cell surface Con A from intracellular lectin. Labeling at 4 degrees C resulted in a uniform surface distribution of Con A irrespective of cell size. After a 1-hr incubation of Con A-labeled cells in lectin-free medium at 37 degrees C, lower epidermal cells and approximately half of middle epidermal cells internalized Con A/receptor complexes by endocytosis while lectin remained diffusely on the remainder of middle epidermal cells and upper epidermal cells. By electron microscopy, ferritin-Con A was clustered on surface areas and invaginations of the plasma membrane before being endocytosed. We concluded that the differentiation of epidermal cells was accompanied by progressive decrease in endocytosis and, most probably, mobility of Con A receptors.

Animals↗
PubMed1983

Potassium iodide in erythema nodosum and other erythematous dermatoses.

Potassium iodide therapy has a history of more than 150 years. It has been tried in many diseases in the past. However, with the development of modern medications indications for potassium iodide therapy are very limited. It is well known that potassium iodide is the drug of choice for sporotrichosis. Subacute nodular migratory panniculitis and erythema nodosum have also been treated successfully with this drug.

Erythema Multiforme↗
PubMed1983

The alterations of keratinocyte surface and basement membrane markers by treatment with 8-methoxypsoralen plus long-wave ultraviolet light.

The alterations of keratinocyte surface and basement membrane markers by treatment with 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet (UVA) light (PUVA) were examined in guinea pig skin using immunofluorescence (IF) microscopy. Following a single PUVA treatment (UVA doses: 1.8 - 7.2 J/cm2), reactivity with pemphigus and pemphigoid sera, rabbit anti-guinea pig epidermal cell serum, and fluorescein-conjugated concanavalin A was decreased in intensity in a dose-dependent fashion. Fluorescence became distinctly less pronounced by day 2 postirradiation and recovered between days 6-10. IF with rabbit antiglomerular basement membrane antibodies, which cross-reacted with the basement membrane of the skin, apparently was unaltered within this energy dose range. 8-MOP or UVA alone did not change the reactivity with any reagent. These results suggest that PUVA treatment affects keratinocyte membrane markers and pemphigoid antigens but not some of the basement membrane antigens.

Animals↗
PubMed1983

Topical 8-methoxypsoralen photochemotherapy of psoriasis: a clinical study.

Topical psoralen plus UV-A irradiation (topical PUVA) was re-evaluated with regard to the timing of UV-A exposure. Symmetrical lesions of fifteen patients with psoriasis were treated with topical PUVA. One side was exposed to UV-A 2 h after topical application of I% 8-methoxypsoralen (2-h interval therapy), while the other side was exposed to the same dose of UV-A within 5 min of the topical application (non-interval therapy). Both regimens were effective. The non-interval therapy was preferred in one case, the 2-hour interval was preferred in three cases, and there was no clear difference in the other eleven cases. There was less tendency to burning with the non-interval therapy, and our study suggests that this is a useful regimen in the out-patient treatment of psoriasis.

Administration, Topical↗
PubMed1983

Distribution patterns of cytoplasmic microtubules in epidermal keratinocytes.

The distribution of cytoplasmic microtubules in cultured guinea-pig keratinocytes was investigated using immunofluorescence (IF) microscopy with monospecific anti-tubulin antibodies and electron microscopy (EM). In culture, adherent cells displayed networks of thin fluorescent fibres, while a homogeneous and/or granular cytoplasmic IF was shown in the cells of upper layers as well as in trypsinized cells. By EM many microtubules were shown in adherent cells but there were fewer or none in the upper layers. An increase in calcium ion (Ca2+) concentration and the addition of an ionophore (X537A) to the culture medium caused disassembly of microtubules. This effect was cancelled by a calmodulin inhibitor. Cryostat sections of normal human and guinea-pig epidermis stained with anti-tubulin antibodies showed a homogeneous and/or granular cytoplasmic IF from basal to granular layers but no detectable IF was seen in the horny layer. These results suggest that keratinocytes contain a cellular pool of tubulin in various states of polymerization and that microtubule disassembly may occur during differentiation, probably being regulated by Ca2+-calmodulin complexes.

Animals↗
PubMed1982

Bullous pemphigoid and antinuclear antibodies. Unmasking of basement membrane fluorescence in sodium chloride-treated substrates.

Immunoflourescent (IF) microscopic studies were done on a patient with bullous pemphigoid who had a high titer of antinuclear antibodies (ANAs). Direct IF microscopy showed deposition of lgG and C3 at the basement membrane zone (BMZ), while, by indirect IF microscopy, ANAs (but not circulating pemphigoid antibodies) were detected. The 2M sodium chloride (NaCl) solution-treated substrates, in which nuclear antigens were eluted, uncovered pemphigoid antibodies. Treatment of the substrates with NaCl solution unmasked BMZ fluorescence in another set of experiments in which a large amount of serum samples containing ANAs was added to serum samples containing only pemphigoid antibodies. These results suggest that pemphigoid antibodies are able to react to the BMZ in the presence of concomitant ANAs unless bind to the nuclear antigens.

Animals↗
PubMed1982

Assessment of anti-stratum corneum antibody titres in pustulosis palmaris et plantaris.

Titres of anti-stratum corneum (SC) antibodies, determined by an indirect immunofluorescence (IF) technique, were significantly higher on average in pustulosis palmaris et plantaris (PPP) and pompholyx than in normal controls. By a complement IF technique, the antibodies fixed complement (C3) in high titer in PPP, but to a much lesser degree in pompholyx and normal controls. Direct IF microscopy studies showed the deposition of IgG and C3 in the SC in some of the biopsy specimens of the pustular lesions. These findings suggest that in PPP anti-SC antibodies may be involved at least in part in activation of the complement system and the subsequent accumulation of polymorphonuclear leukocytes.

Antibodies↗
PubMed1982

Formation of UV-induced apoptosis relates to the cell cycle.

The relationship of the rate of epidermal proliferation to ultraviolet (UV)-induced cell death, namely sunburn cell (SC) formation, was investigated in vivo using the guinea-pig model. The number of SCs was correlated with (1) cellophane tape stripping which stimulates the proliferation rate and (2) treatment with antimitotic and antimetabolic agents which suppress the proliferation rate. The tape stripping performed 14 h before UV irradiation significantly increased the number of SCs counted 24 h after UV irradiation from a mean of 17.4 to 62.6 per section, and the tritiated thymidine (TdR-3H)-labelling index (LI) increased from a mean of 8.1 to 27.4%. SC counts and LI were markedly decreased by the intradermal injection of colchicine, methotrexate, hydroxyurea or 5-fluorouracil given once immediately after the tape stripping. The autoradiographic study showed that 23.2% of SCs were labelled when TdR-3H was given intradermally 1 h before UV exposure, while no SCs were labelled when TdR-3H was given immediately after UV exposure. The labelled SC count (23.2%) which presumably represents S phase cells at the time of UV exposure, was higher than the LI (mean 8.1%). These results suggest that proliferating cells, possibly S phase cells, may be responsible for SC formation.

Animals↗
PubMed1982

Deposition of complement C1q in primary localized cutaneous amyloidosis.

Deposition of immunoglobulins and complement components was studied in twelve cases of primary localized cutaneous amyloidosis by direct immunofluorescence microscopy. C1q was detected in amyloid islands in ten cases by immunoglobulins and C3 were found in only a few cases. It is suggested that C1q may be one of the nonepidermal components of cutaneous amyloid.

Amyloidosis↗
PubMed1982

Squamous cell carcinoma associated with disturbance of the IgA system.

A case of cell carcinoma of the skin associated with disturbance of the IgA system is described. Immunological observations revealed a marked low level of serum IgA and disturbance of the secretory IgA synthesis in the rectal mucosa. After the surgical removal of the skin tumor, the serum level of IgA was increased to half the normal-range level. The relationship of the disturbance of the IgA system to the occurrence of squamous cell carcinoma is discussed.

Aged↗