Dermal anchoring structures: convex matrix structures at the bottom of the dermal layer that contribute to the maintenance of facial skin morphology.

BACKGROUND/PURPOSE: Facial skin must be linked to underlying structures to maintain facial morphology and prevent sagging, but the mechanism of facial skin retention is largely unknown. We aimed to elucidate this mechanism. METHODS: Twenty-two cheek skin specimens (age range: 10s-60s, both genders) were observed histologically. And 30 cheek of healthy Japanese volunteers (age range: 30s-50s, female) was photographed and the severity of sagging was graded. Dermal layer morphology was observed non-invasively with ultrasound. Skin-retaining force was measured with a Cutometer MPA 580(®) , and sagging severity was evaluated by grading criteria. RESULTS: Histological observation revealed characteristic convex structures at the bottom of the dermal layer. Non-invasive study showed that the depth of the convex structures, measured by ultrasonography, was significantly negatively related to the ratio of viscoelastic to elastic distention (Uv/Ue) and positively related to the ratio of elastic recovery to total deformation (Ur/Uf) at the cheek of female volunteers, measured by cutometer. It was also negatively related to sagging severity. Further, Ur/Uf was negatively and Uv/Ue was positively related to sagging severity. CONCLUSION: Characteristic convex structures at the bottom of the dermal layer serve as anchoring structures to maintain skin morphology.

The ability of four catechol estrogens of 17beta-estradiol and estrone to induce DNA adducts in Syrian hamster embryo fibroblasts.

Catechol estrogens are considered critical intermediates in estrogen-induced carcinogenesis. We demonstrated previously that 17beta-estradiol (E(2)), estrone (E(1)) and four of their catechol estrogens, 2- and 4-hydroxyestradiols (2- and 4-OHE(2)), and 2- and 4-hydroxyestrones (2- and 4-OHE(1)) induce morphological transformation in Syrian hamster embryo (SHE) fibroblasts, and the transforming abilities vary as follows: 4-OHE(1) > 2-OHE(1) > 4-OHE(2) > 2-OHE(2) vertical line E(2), E(1). To examine the involvement of catechol estrogens in the initiation of hormonal carcinogenesis, we studied the ability of E(2), E(1) and their catechol estrogens to induce DNA adducts in SHE cells by using a (32)P-post-labeling assay. DNA adducts were detected in cells treated with each of all the catechol estrogens at concentrations of 10 microg/ml for 1 h and more. 2- or 4-OHE(2) formed a single DNA adduct, which was chromatographically distinct from each other. In contrast, 2- or 4-OHE(1) produced one major and one minor adduct, and the two adducts formed by each catechol estrogen exhibited identical mobilities on the chromatograms. Neither E(2) nor E(1) at concentrations up to 30 microg/ml induced DNA adducts. The abilities of the estrogens to induce DNA adducts were ranked as follows: 4-OHE(1) > 2-OHE(1) > 4-OHE(2) > 2-OHE(2) > > E(2), E(1), which corresponds well to the transforming and carcinogenic abilities of the estrogens. In addition, the level of DNA adducts induced by the catechol estrogens was markedly decreased by co-treatment of cells with the antioxidant L-ascorbic acid. The results indicate the possible involvement of oxidative metabolites of catechol estrogens of E(2) and E(1) in the initiation of endogenous estrogen-induced carcinogenesis.

The expression of PPAR-associated genes is modulated through postnatal development of PPAR subtypes in the small intestine.

In this study, we found that the mRNA level of peroxisome proliferator-activated receptor (PPAR) alpha, but not of PPARdelta, was elevated in the jejunum during the postnatal development of the rat. Moreover, we found that the expressions of PPAR-dependent genes, such as acyl-CoA oxidase, L-FABP, and I-FABP, were also increased during the postnatal development of the small intestine. Electrophoretic mobility shift assay revealed that both the PPARalpha-9-cis-retinoic acid receptor alpha (RXRalpha) heterodimer and the PPARdelta-RXRalpha heterodimer bound to the peroxisome proliferator response element (PPRE) of acyl-CoA oxidase and L-FABP genes. The binding of the PPARalpha-RXRalpha heterodimer to the PPREs of the various genes was enhanced by the addition of PPARalpha, with a concomitant reduction of the binding of PPARdelta-RXRalpha to the PPREs. Furthermore, the binding activity of PPARalpha-RXRalpha, but not PPARdelta-RXRalpha, to the PPREs was enhanced by the addition of a PPAR ligand, WY14,643. The GAL4-PPAR-chimera reporter assay showed that WY14,643 transactivated the reporter gene through action of PPARalpha, but not through PPARdelta, in Caco-2 cells. Furthermore, oral administration of a PPAR ligand, clofibrate, during 3 consecutive days of the weanling period caused a parallel increase in the mRNA levels of these PPAR-dependent genes. These results suggest that acyl-CoA oxidase, L-FABP and the other PPAR-dependent genes in the small intestine may be coordinately modulated during postnatal development by the disproportional expression of PPARalpha over PPARdelta.

Delayed induction of pigmented spots on UVB-irradiated hairless mice.

Human skin exposed to solar radiation for a long time subsequently develops pigmented spots, which are named solar lentigines. Since no animal model of this process is currently available, we attempted to induce similar spots in pigmented hairless mice. The mice were irradiated at 38 or 94 mJ/cm(2) three times/week for various periods of time (1-8 weeks) under an ultraviolet light source (Toshiba FL-SE; UVB). Skin pigmentation of irradiated mice was visually observed and skin color was determined with a colorimeter for 78 weeks. Uniform pigmentation was induced, but persisted only during exposure, disappearing completely within 2 weeks after cessation of exposure. At about 28 weeks after the first exposure, pigmented spots suddenly began to appear. These pigmented spots were less than 2 mm in diameter and light brown in color. The length of the latent period until appearance and the extent of development of these spots were dependent on the exposure period. Histological examination revealed increased numbers of active melanocytes and melanin granules in the affected epidermis. These pigmented spots closely resemble solar lentigines in humans, and the mice should be useful as an animal model of solar lentigines.

Three-dimensional evaluation of lumbar disc hernia and prediction of absorption by enhanced MRI.

Both the spontaneous shrinkage and the disappearance of disc hernia have been confirmed through the use of computed tomography (CT) and magnetic resonance imaging (MRI). There is, however, no practical method to predict the likely absorption of the herniated mass. The objective of this study was to predict the spontaneous absorption of disc hernia by MRI, and to select the optimum treatment. The study involved 65 patients with lumbar disc hernias. Conservative treatment was carried out in 21 patients, while 44 patients underwent herniotomy. In the nonoperated patients, an MRI was taken both during the painful period, and shortly after pain remission. Hernial shrinkage was evaluated according to the decrease in the calculated volume, in addition to the decrease in hernial area, calculated by MRI. In the operated group, preoperative MRI enhancement, type of hernia, and invasion of granulation tissue in the histological specimens were studied. In the 21 nonoperated patients, the volume (mean +/- SD) was 0.488 +/- 208 cm(3) (range, 0.197-0.931 cm(3)) in the painful period and 0.214 +/- 0.181 cm(3) (range, 0.0-0.744 cm(3)) in the remission period. This decrease in volume was statistically significant. There was also a greater decrease in hernias exhibiting positive enhancement by MRI. In the operated patients, hernias that penetrated the posterior longitudinal ligament (PLL) had high rates of preoperative enhancement, and these hernias showed invasion of granulation tissue with marked neovascularization. Positive enhancement by MRI confirms an ongoing absorption process. Enhanced MRI can be a good method for the prediction of spontaneous absorption of lumbar disc hernias.

Involvement of genotoxic effects in the initiation of estrogen-induced cellular transformation: studies using Syrian hamster embryo cells treated with 17beta-estradiol and eight of its metabolites.

To examine a direct involvement of genotoxic effects of estrogens in the initiation of hormonal carcinogenesis, the abilities of 17beta-estradiol (E2) and 8 of its metabolites to induce cellular transformation and genetic effects were studied using the Syrian hamster embryo (SHE) cell model. Treatment with E2, estrone (E1), 2-hydroxyestrone (2-OHE1), 4-hydroxyestrone (4-OHE1), 2-methoxyestrone (2-MeOE1), 16alpha-hydroxyestrone (16alpha-OHE1), 2-hydroxyestradiol (2-OHE2), 4-hydroxyestradiol (4-OHE2) or estriol (E3) for I to 3 days inhibited SHE cell growth in a concentration-dependent manner. Concentration-dependent increases in the frequency of morphological transformation in SHE cells were exhibited by treatment for 48 hr with each of all estrogens examined, except for E3. The transforming activities of the estrogens, determined by the induced transformation frequencies, were ranked as follows: 4-OHE1 > 2-OHE1 > 4-OHE2 > 2-OHE2 > or = E2 or E1 > 2-MeOE1 or 16alpha-OHE1 > E3. Somatic mutations in SHE cells at the Na+/K+ATPase and /or hprt loci were induced only when the cells were treated with 4-OHE1, 2-MeOE1 or 4-OHE2 for 48 hr. Some estrogen metabolites induced chromosome aberrations in SHE cells following treatment for 24 hr. The rank order of the clastogenic activities of the estrogens that induced chromosome aberrations was 4-OHE1 > 2-OHE1 or 4-OHE2 > 2-OHE2 > E1. Significant increases in the percentage of aneuploid cells in the near diploid range were exhibited in SHE cells treated for 48 hr or 72 hr with each of the estrogens, except for 4-OHE1 and E3. Our results indicate that the transforming activities of all estrogens tested correspond to at least one of the genotoxic effects by each estrogen, i.e., chromosome aberrations, aneuploidy or gene mutations, suggesting the possible involvement of genotoxicity in the initiation of estrogen-induced carcinogenesis.

[Unexpected hyperkalemia during general anesthesia in three patients undergoing hepatic, cholangioler or pancreatic surgery].

Three patients developed unaccountable hyperkalemia during general anesthesia for pancreatectomy, hepatectomy, and cholangio-jejunostomy. The patients had normal preoperative renal function, serum potassium values, and intraoperative urine output. The surgical manipulations might have reduced portal venous and/or hepatic arterial blood flow resulting in the hepatic ischemia. Consequently, hepatic intra-cellular potassium might have leaked into the blood causing hyperkalemia. Anesthesiologists should be aware of the potential risk of hyperkalemia caused by surgical interventions on the liver and/or pancreas.

Bisphenol-A induces cellular transformation, aneuploidy and DNA adduct formation in cultured Syrian hamster embryo cells.

Bisphenol-A (BP-A) is a major component of epoxy, polycarbonate and other resins. For an assessment of in vitro carcinogenicity and related activity of BP-A, the abilities of this compound to induce cellular transformation and genetic effects were examined simultaneously using the Syrian hamster embryo (SHE) cell model. Cellular growth was reduced by continuous treatment with BP-A at doses > or = 100 microM. However, colony-forming efficiencies were not decreased significantly following treatment with up to 200 microM BP-A for 48 hr. Morphological transformation of SHE cells was induced by treatment of cells with BP-A at 50 to 200 microM for 48 hr. BP-A exhibited transforming activity at doses > or = 50 microM but was less active than the benzo[alpha]pyrene used as a positive control. Over the dose range that resulted in cellular transformation, treatment of SHE cells with BP-A failed to induce gene mutations at the Na+/K+ ATPase locus or the hprt locus. No statistically significant numbers of chromosomal aberrations were detected in SHE cells treated with BP-A. However, treatment of cells with BP-A induced numerical chromosomal changes in the near diploid range at doses that induced cellular transformation. 32P-Postlabeling analysis revealed that exposure of cells to BP-A also elicited DNA adduct formation in a dose-dependent fashion. Our results indicate that BP-A has cell-transforming and genotoxic activities in cultured mammalian cells and potential carcinogenic activity.

Cell-transforming activity and genotoxicity of phenolphthalein in cultured Syrian hamster embryo cells.

Phenolphthalein is a cathartic agent widely used in non-prescription laxatives. For the simultaneous assessment of in vitro carcinogenicity and mutagenicity of phenolphthalein, the ability of this chemical to induce cell transformation and genetic effects was examined using the Syrian hamster embryo (SHE) cell model. Cell growth was reduced by treatment with phenolphthalein at 10-40 microM in a dose-related manner. Treatment with phenolphthalein for 48 hr induced a dose-dependent increase in morphological transformation of SHE cells. Over the dose range that resulted in cell transformation ( 10-40 microM), treatment of SHE cells with phenolphthalein induced gene mutations at the hprt locus but not at the Na+/K+ ATPase locus. A statistically significant level of chromosomal aberrations was elicited in SHE cells treated with phenolphthalein at the highest dose (40 microM). Meanwhile, neither numerical chromosomal changes nor DNA adduct formation, analyzed by the nuclease P1 enhancement version of 32P-post-labeling, were induced by treatment with phenolphthalein at any concentrations examined. We thus report cell-transforming activity and mutagenicity of phenolphthalein assessed with the same mammalian cells in culture. Our results provide evidence that phenolphthalein has cell-transforming and genotoxic activity in cultured mammalian cells. The mutagenic and clastogenic activities of phenolphthalein could be a causal mechanism for carcinogenicity in rodents.

Primary cutaneous Ki-1+ anaplastic large cell lymphoma: a morphologic, immunohistochemical and genetic study of an indolent case.

A 59-year-old woman with a large nodular ulcerative lesion on her neck was presented. She had a 3 year history of recurrent cutaneous nodules which spontaneously regressed before regional lymphadenopathies appeared. She has followed an indolent clinical course for seven years after the first overt lymphadenopathies appeared. Histological findings were compatible with anaplastic large cell lymphoma (ALCL). The tumor cells strongly expressed Ki-1 (CD30), HLA-DR, IL-2 receptor (CD25) and leukocyte common antigen. These findings led to the diagnosis of primary cutaneous Ki-1+ ALCL. Although the majority of the tumor cells did not express T-cell related antigens, the detection of monoclonal TCR gene rearrangement clearly established the T-cell lineage nature.

[Immediate hypersensitive reactions to the ingestion of egg white and IgE binding to the egg white components].

IgE is considered to be involved in immediate hypersensitive reactions (IHR) following egg ingestion. IgE antibody levels to egg-white (EW) antigens in the IHR-positive group (n = 19, mean age +/- SD = 5.2 +/- 4.5 yr) were higher than those in the IHR-negative group (n = 13, mean of age +/- SD = 3.6 +/- 2.2 yr). However, even in the IHR-negative group, some patients showed high IgE to EW. RAST inhibition tests with heat-treated (100 degrees C, 5, 10, and 30 min) egg-white antigens were performed on 13 serum samples from subjects with IHR and 9 serum samples from subjects without IHR. Heat treatment decreased the IgE-binding activity of egg white and it was speculated that IgE from IHR-negative subjects bound to relatively heat-unstable sites of egg-white antigens. Furthermore, we selected IHR-negative subjects (n = 8, mean of age +/- SD = 3.0 +/- 1.7 yr) with higher IgE antibody levels than the lowest limit of IgE to EW of the IHR-positive group and compared IgE to ovomucoid (OM), ovalbumin (OA), conalbumin (CA), and lysozyme (Ly) between these IHR-negative and positive groups. IgE-binding activities to egg-white components, including OA, CA, and Ly but not OM, were significantly decreased with heat treatment. The IHR-negative group showed significantly lower IgE to OM (untreated, 5, 10, 30 min treatment) and 5 min treated OA alone than the IHR-positive group, while no difference was found in IgE to other components between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Elucidation of chemical compounds responsible for foot malodour.

Short-chain fatty acids from the socks and feet of subjects either with strong foot odour or with weak or no foot odour were extracted with ethyl ether, and then analysed by gas chromatography/mass spectrometry (GC/MS). Short chain fatty acids were found in greater amounts from those subjects with strong foot odour. Iso-valeric acid was present in all the subjects with foot odour but was not detected in those without. Olfactory evaluations of the various short-chain fatty acid solutions were in agreement with the GC/MS analyses. By incubating sweat and lipid from subjects with strong foot odour, we succeeded in reproducing the foot malodour. GC/MS analyses of reproduced foot odour revealed that short-chain fatty acids were present in a similar composition to that found in vivo.