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We previously revealed that the mechanism of demosponge skeleton construction is self-organization by multiple rounds of sequential mechanical reactions of player cells. In these reactions, "transport cells" dynamically carry fine skeletal elements (spicules) on epithelia surrounding the inner body space of sponges (basal epithelium (basopinacoderm) and the endodermal epithelium (ENCM)). Once spicules pierce ENCM and apical pinacoderm, subsequently they are cemented to the substratum under the sponge body, or connected to other skeleton-constructing spicules. Thus, the "pierce" step is the key to holding up spicules in the temporary periphery of growing sponges' bodies. Since sponges can regress as well as grow, here we asked how skeleton construction occurs during local regression of the body. We found that prior to local basopinacoderm retraction (and thus body regression), the body became thinner. Some spicules that were originally carried outward stagnated for a while, and were then carried inwards either on ENCM or basopinacoderm. Spicules that were carried inwards on ENCM pierced epithelia after a short transport, and thus became held up at relatively inward positions compared to spicules carried on outwardly extending basopinacoderm. The switch of epithelia on which transport cells migrate efficiently occurred in thinner body spaces where basopinacoderm and ENCM became close to each other. Thus, the mechanisms underlying this phenomenon are rather mechanical: the combination of sequential reactions of skeleton construction and the narrowed body space upon local retraction of basopinacoderm cause spicules to be held up at more-inward positions, which might strengthen the basopinacoderm's attachment to substratum., (© 2019 Japanese Society of Developmental Biologists.)

Four cases of Hypertrophic Lupus Erythematosus (HLE) were reported. The lesions of HLE were observed on the forearms, face and hands in all four cases. Clinically, the lesions were erythematous, hyperkeratotic plaques. The clinical course was marked by chronicity and progression of the lesion. Histologically, marked hyperkeratosis, parakeratosis, acanthosis, degenerative changes of basal cells in H/E stain, and thickened, multilayered basement membrane in PAS stain, were observed. The observations of Dylon stain revealed that localized amyloid deposition was observed in all four cases of HLE lesions, as fluorescent-orange colored amyloid deposits in the papillary dermis and subepidermal areas at near orjust below the dermo-epidermal junction appeared under fluorescent microscope. On the basis of clinical and histological observations, we suggest that chronic irritation, such as sunlight exposure over a long-duration, might have caused the characteristic abnormalities at the dermo-epidermal junction and also initiated the frequency of amyloid deposits locally secondary to the diseases. We compared our HLE cases to other types of lupus erythematosus (LE) skin lesions, as to whether deposition of amyloid materials were frequently observed or not. Amyloid deposition was observed in one case of DLE and none of the SLE cases. Localized amyloid deposition was more frequently observed in skin lesions, secondary to HLE disease, as compared to other types of LE.

UV radiation suppresses the immune response, a fact which raises the question of whether the phenomenon may find practical applications in the outcome of infectious diseases. In this study, BALB/c mice were exposed to low-dose UVB (250 J/m(2)) from Dermaray M-DMR-100 for 4 consecutive days. Twelve hours after the last UV exposure, groups of mice were injected with 2 x 10(6) Leishmania amazonensis promastigotes. The development of skin lesions, as assessed by measurement of visible cutaneous lesions, was significantly suppressed in low-dose UVB-irradiated mice compared to nonirradiated controls. In order to characterize the cytokines involved in this phenomenon, BALB/c mice were irradiated with identical doses of UVB, and gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin 4 cytokine levels in blood serum and skin were examined at different times by a sandwich enzyme-linked immunosorbent assay, immunohistochemical analysis, and reverse transcription (RT)-PCR. Upregulated expression of serum IFN-gamma and TNF-alpha was observed from 6 to 24 h. Positive results for IFN-gamma and TNF-alpha in UVB-irradiated mice were obtained by immunohistochemical analysis. By RT-PCR, the mRNA expression of both IFN-gamma and TNF-alpha cytokines was detected in a time-dependent manner only in UVB-irradiated mice. Histopathological analysis and electron microscopy revealed that cellular infiltration, tissue parasitism, and parasitophorus vacuoles in irradiated mice were markedly less noticeable than those in nonirradiated controls. These results suggested that low-dose UVB irradiation played a pathogen-suppressing role in Leishmania-susceptible BALB/c mice via systemic and local upregulation of Th1 (IFN-gamma and TNF-alpha) cytokines.

In this study, detection rates of Leishmania parasites from human skin were compared among three different types of specimens, formalin-fixed, ethanol-fixed, and frozen, by polymerase chain reaction (PCR) and Southern blotting. For this purpose, we used biopsy specimens collected from 19 leishmaniasis patients and performed PCR and Southern hybridization with the probe specific for Leishmania (Viannia) braziliensis complex. Among these 19, 16 specimens were from cutaneous leishmaniasis (CL), one, diffuse cutaneous leishmaniasis (DCL) and 2, mucocutaneous leishmaniasis (MCL) and were formalin-fixed and paraffin-embedded. The causative agents for one case of CL and one case of DCL were already identified as L. (Leishmania) complex. Six specimens of CL were preserved in 100% ethanol. Two specimens of MCL were frozen tissues. PCR using the formalin-fixed and paraffin-embedded specimens revealed positive bands at 70 bp in 9 (47.4%) out of 19 specimens of CL, MCL and DCL. Southern blotting detected the signals in 12 (63.2%) out of the 19. PCR using the 100% ethanol-fixed specimens revealed positive bands in 4 (66.7%) out of 6, and Southern blotting also detected the signals in 4 (66.7%) out of the 6. PCR and Southern blotting using 2 frozen specimens of MCL were always positive (100%). Although we failed to detect significant differences by Chi-square test between the results from the formalin-fixed, paraffin-embedded specimens and those from 100% ethanol-fixed ones, we concluded that ethanol-fixed specimens, convenient for transportation and storage, would be more useful for diagnosis of leishmaniasis by PCR in a developing country.

Porphyrins are fluorescent chemicals excited by visual light. Skin changes in patients with porphyrias develop when the skin is exposed to sunlight and porphyrins have precipitated. This reaction is phototoxic. Since the phototoxic reaction varies with each porphyria, each porphyria demonstrates different skin changes. Conversely, skin changes do not develop if skins are completely protected from exposure to the sun in patients with porphyrias with show severe abnormalities in the metabolism of porphyrin pathways. In Japan, relatively popular porphyrias in dermatology clinic are porphyria cutanea tarda (PCT), erythropoietic protoporphyria (EPP) and congenital erythropoietic porphyria (CEP). Histopathologically, one of the most important findings in porphyria is a deposition of PAS positive materials at the dermo-epidermal junction and around the small blood vessels in the dermis.

Chronic verruga nodules taken from a patient with Bartonellosis (verruga peruana) were studied. Histologically, specimens of all the verruga nodules had features consistent with granulomatous lesions with extensive infiltration of various types of cells along with the proliferation of capillaries. The sections were predominantly infiltrated with neutrophils and endothelial cells; histiocytes, plasma cells, lymphocytes and mast cells were also visible to some extent. The blood vessels were dilated, and many rounded and swollen endothelial cells were located peripherally; a huge number of neutrophils invaded the vessels. Electron microscopically, large number of organisms were seen in different stages of the life cycle in the stroma. Furthermore, organisms were regularly seen either in close contact or existing inside the cytoplasm of neutrophils, suggesting the phagocytic role of these cells. No organism was found inside any endothelial cells or histiocytes.

The relationship between PCBs and PCQs concentrations in the skin surface lipids and blood was investigated in this study. PCBs and PCQs concentrations in thirty two patients with PCB poisoning (Yusho) and 20 normal controls were analyzed. The collection of skin surface lipids was performed by the method of cotton pad with 70% ethyl alcohol. The alkaline decomposition method described in the official standard analytical methods for the isolation of PCBs and PCQs fractions was used. In the blood of control group, mean value of PCBs concentration was 2.1 ng/g, and that of PCQs concentration was too low to be detected by our analytical method. On the other hand, the PCBs concentration in the Yusho group were two times higher than those in the control group. The mean value of PCQs concentration was 0.90 ng/g in Yusho group, while it was not detectable in the control group. In the skin surface lipids of patients with Yusho, the mean value of PCBs concentration was 580.0 ng/g, but was 324.4 ng/g in the control group. The mean value of PCQs concentration in the skin surface lipids of Yusho patients was 25.7 ng/g, although it was not detected in the control group. PCBs and PCQs levels in the skin surface lipids were higher than those in the blood. This means that cutaneous sebaceous system is one of the excreted systems of polyhalogenated chemicals, such as PCBs or PCQs, when these chemicals are precipitated in human or mammalians.

The magnitude and time course of UV radiation-induced photoprotection was investigated in fair-skinned volunteers. Resistance to sunburn was evident three days following single exposures to UV-B, reached a maximum by seven days, and declined gradually over a period of 30 to 40 days. Both the magnitude and time course of UV radiation-induced photoprotection were dose related. The maximal mean protection factor following an exposure to 2 minimal erythemal doses was 4.2. The present findings, along with earlier studies, suggest that there are pronounced spectral differences with regard to the induction of photoprotective adaptation and that UV-B wavelengths are the most effective.

The degree of complement activation produced by hydrogen peroxide was estimated by the inhibition of serum homolytic activity (% IHA). Sera from patients with systemic lupus erythematosus and psoriasis vulgaris were resistant to hydrogen-peroxide-mediated complement activation. %IHA negatively correlated with ceruloplasmin level or catalase activity in systemic lupus erythematosus sera, but did not correlate with transferrin level. The addition of free metal ions, FeCl2 or CuCl2, promoted hydrogen-peroxide-mediated complement activation. These results suggest that hydroxyl radical is involved in complement activation and that the factors responsible for the insensitivity of pathological sera to H2O2 are catalase and ceruloplasmin in the sera. Human skin fibroblasts generate superoxide and tumor necrosis factor enhanced it, but interleukin-1 beta inhibited it. Normal serum cultured with fibroblasts for 24 h showed complement activation via catalase-inhibitable process, suggesting that hydrogen peroxide has an important role in fibroblast-mediated complement activation. It is speculated that fibroblasts and complement activation by oxygen radicals have an important role in inflammation and subsequent tissue damage at the site of skin lesion.