Urban Tree Canopy and Environmental Justice: Examining the Distributional Equity of Urban Tree Canopy in Guangzhou, China.

Rapid urbanization has led to a series of environmental problems that are harmful to the physical and mental health of residents. Not only can increasing urban tree canopy (UTC) improve sustainable city development, but it can also effectively promote the quality of life for residents; however, the uneven spatial distribution of UTC can also bring about social justice problems. Currently, there are few studies related to the justice of UTC distribution in China. Based on this, the paper adopts object-oriented image classification technology to interpret and extract UTC data from satellite images, and it uses house price to explore the justice of the spatial distribution of UTC in the main urban area of Guangzhou from the perspective of environmental justice by ANOVA, Pearson correlation coefficient, and bivariate local spatial autocorrelation. The results show that: (1) There is a significant positive correlation between UTC and house price in the main urban area of Guangzhou, and there are regional differences in the distribution of UTC, with the UTC in the "very high" house price group being significantly higher than that in other groups. (2) The spatial clustering of UTC and house price in the main urban area of Guangzhou is found to be "low-low" and "high-high"; thus, it can be concluded that the spatial distribution of UTC in the main urban area of Guangzhou is uneven. This is an environmental injustice, as the areas with low UTC are spatially clustered in old residential areas, while the areas with high UTC are spatially clustered in commercial housing estates with high house prices. The study shows that urban tree planting should not only focus on quantitative improvement but also on equitable spatial layouts to promote social equity and justice thereby improving the urban ecological environment and promoting healthy urban development.

A partially penalty immersed Crouzeix-Raviart finite element method for interface problems.

The elliptic equations with discontinuous coefficients are often used to describe the problems of the multiple materials or fluids with different densities or conductivities or diffusivities. In this paper we develop a partially penalty immersed finite element (PIFE) method on triangular grids for anisotropic flow models, in which the diffusion coefficient is a piecewise definite-positive matrix. The standard linear Crouzeix-Raviart type finite element space is used on non-interface elements and the piecewise linear Crouzeix-Raviart type immersed finite element (IFE) space is constructed on interface elements. The piecewise linear functions satisfying the interface jump conditions are uniquely determined by the integral averages on the edges as degrees of freedom. The PIFE scheme is given based on the symmetric, nonsymmetric or incomplete interior penalty discontinuous Galerkin formulation. The solvability of the method is proved and the optimal error estimates in the energy norm are obtained. Numerical experiments are presented to confirm our theoretical analysis and show that the newly developed PIFE method has optimal-order convergence in the [Formula: see text] norm as well. In addition, numerical examples also indicate that this method is valid for both the isotropic and the anisotropic elliptic interface problems.

Suppressive effect of administration of recombinant human thioredoxin on cutaneous inflammation caused by UV.

Thioredoxin (TRX) is small ubiquitous protein, which regulates cellular redox status and scavenges reactive oxygen species (ROS). TRX has been shown to exert suppressive effect on skin inflammation where oxidative stress is involved in its pathogenesis. We investigated the effect of TRX on UVB response. Ear swelling after UVB irradiation was significantly reduced in TRX-transgenic mouse compared with wild-type mouse. Furthermore, we have demonstrated that intraperitoneal administration of recombinant human thioredoxin (rhTRX) also reduced acute skin inflammatory reaction, such as skin erythema and edema. Histologically, inflammatory cells including neutrophils and lymphocytes were significantly reduced and average size of the caliber of blood vessels were also reduced in rhTRX-injected mice. The number of apoptotic keratinocytes, were significantly reduced in rhTRX-injected mice. Immunohistochemical intensity of 8-hydroxy-2'-deoxyguanosine was strikingly reduced in rhTRX-injected mouse. Western blotting showed that administration of rhTRX inhibited phosphorylation of p38 mitogen-activated protein kinases and c-Jun NH 2-terminal kinase, which play important roles in inflammatory and apoptotic signaling. These findings indicated that rhTRX attenuated inflammatory and apoptotic responses by UVB. Possible mechanisms for this might be via redox regulation of stress signaling and reduction of reactive oxygen species. We discussed the future use of TRX for sedative use of skin inflammation.

Suppressive effect of recombinant human thioredoxin on ultraviolet light-induced inflammation and apoptosis in murine skin.

Thioredoxin (TRX) is a small ubiquitous protein, which regulates cellular redox status and scavenges reactive oxygen species. The present study was conducted to investigate the effect of TRX on ultraviolet (UV)-B-mediated inflammatory and apoptotic responses. Ear swelling after UV-B irradiation was significantly reduced in TRX-transgenic mice compared to wild-type mice. Administration i.p. of recombinant human TRX also reduced acute skin inflammatory reaction, such as skin erythema and swelling. Histologically, numbers of inflammatory cells including neutrophils and lymphocytes were significantly reduced and the average size of the caliber of blood vessels were also reduced in recombinant human TRX-injected mice. The number of apoptotic keratinocytes, in terms of sunburn cells, activated-caspase-3-positive cells and terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells were all significantly reduced in recombinant human TRX-injected mice. Immunohistochemical intensity of 8-hydroxy-2'-deoxyguanosine was strikingly reduced in recombinant human TRX-injected mouse. Western blotting showed that administration of recombinant human TRX attenuated duration of phosphorylation of p38 mitogen-activated protein kinases and intensity of phosphorylation of c-Jun N-terminal kinase in the early phase, which play important roles in inflammatory and apoptotic signaling. Collectively, these findings indicated that recombinant human TRX attenuated inflammatory and apoptotic responses caused by UV-B. Possible mechanisms for this might be via redox regulation of stress signaling and reduction of reactive oxygen species.

Thioredoxin suppresses the contact hypersensitivity response by inhibiting leukocyte recruitment during the elicitation phase.

Thioredoxin, a redox-regulating protein that scavenges reactive oxygen species, appears to show an excellent antiinflammatory effect in treating animal models of various human inflammatory diseases. The aim of this study was to clarify whether thioredoxin is useful for treating inflammatory skin diseases, such as contact dermatitis, caused by epicutaneous exposure to environmental and occupational antigens. The allergic contact hypersensitivity response was suppressed in thioredoxin-transgenic mice. This suppressive effect of thioredoxin appeared to be via the inhibition of the efferent limb of contact hypersensitivity because administration of recombinant thioredoxin suppressed the inflammatory response in the elicitation phase but not in the induction phase. Adoptive-transfer studies revealed that the host environment, but not donor leukocytes, is critical in this suppressive effect. In thioredoxin-transgenic mice, the infiltration of neutrophils in the elicitation site was diminished, whereas the migratory function of cutaneous dendritic cells and hapten-specific cell proliferation were not disturbed. Thioredoxin-transgenic mice had also an attenuated inflammatory response to croton oil. These findings suggest that thioredoxin prevents skin inflammatory responses and could be a suitable candidate for the treatment of contact dermatitis.

Acquired unilateral melanocytic nevi in otherwise normal skin.

We describe a case with numerous melanocytic nevi in otherwise normal skin. A 5-year-old girl presented with more than 100 small pigment lesions on her left arm, shoulder and upper back without underlying light brown macule. The pigment lesions were first found on her left forearm at 3 months old and gradually increased along with her growth. Skin biopsy from a pigmented lesion shows a pathological change in compound-type melanocytic nevus without any atypical changes. Speckled lentiginous nevus is known to have multiple melanocytic lesions on the underlying brown macule from birth. Partial unilateral lentiginosis is characterized by unilateral lentigines with histopathological changes in lentigo but not melanocytic proliferation in the dermis. Agminated melanocytic nevi tend to be clustered together in a circumscribed area, whereas in the present case melanocytic nevi were segmentally arranged but not agminated. We consider that this is an unusual type of mosaicism of melanocytic disorders.

Involvement of interleukin-10 promoter polymorphisms in nonmelanoma skin cancers-a case study in non-Caucasian skin cancer patients.

Interleukin 10 (IL-10) is a potent immunosuppressive cytokine, therefore elevated IL-10 expression has been implicated in inhibition of antitumor immune response. IL-10 gene promoter polymorphism has been shown to be involved in susceptibility to skin cancers, but there has been no report focusing on susceptibility to skin cancers among non-Caucasian populations. We enrolled 129 patients with skin cancers and 50 age- and sex-matched healthy controls between April 2004 and March 2007. Genomic DNA was extracted from patients' blood samples and IL-10 promoter polymorphisms were identified using polymerase chain reaction-restriction fragment length polymorphism or direct sequencing. The distribution of the frequency of allele or haplotype of IL-10 gene promoter in Japanese was quite different from that of Europeans. No significant differences could be demonstrated in the frequency of allele or haplotype of IL-10 gene promoter between the patient group and the control group. However, the frequency of the low-IL-10 expression haplotype was significantly high in Bowen's disease subgroup. The frequency of low expression IL-10 promoter genotype was significantly less (P = 0.009, chi(2) = 6.74) in the group of nonmelanoma skin cancer generated on sun-exposed areas in comparison with that on covered areas. Our results indicated that low expression haplotype of IL-10 in Bowen's disease may inhibit the escape of tumor cells from immune surveillance, resulting in suppression of tumor growth and tumor invasion to the dermis. Moreover, high IL-10-expressing haplotype of IL-10 promoter may be a risk factor for photocarcinogenesis.

Src homology 2 domain-containing protein tyrosine phosphatase substrate 1 regulates the induction of Langerhans cell maturation.

Recently, we reported that Src homology 2 domain-containing protein tyrosine phosphatase substrate 1 (SHPS-1) plays an important role in the migration of Langerhans cells (LC). Here, we show that SHPS-1 is involved in the maturation of LC. Immunofluorescence analysis on epidermal sheets for I-A or CD86 revealed that LC maturation induced by 2,4-dinitro-1-fluorobenzene (DNFB) or by TNF-alpha was inhibited by pretreatment with an anti-SHPS-1 monoclonal antibody (mAb) or with CD47-Fc fusion protein, a ligand for SHPS-1. Further, FACS analysis demonstrated that I-A(+) LC that had emigrated from skin explants expressed CD80 or CD86, whereas CD47-Fc protein reduced CD80(high+) or CD86(high+) cells. CD47-Fc protein also reduced the up-regulation of surface CD80 or CD86 by LC remaining in the skin explants. In SHPS-1 mutant mice, we observed that the up-regulation of surface CD86 and CCR7 by LC induced by DNFB as well as that of surface CD80 and CD86 by LC in skin explants was attenuated. Finally, contact hypersensitivity (CHS) response was suppressed in SHPS-1 mutant mice and in wild-type mice treated with an anti-SHPS-1 mAb. These observations indicate that SHPS-1 plays an important role in the maturation of LC ex vivo and in vivo, and that SHPS-1-CD47 interaction may negatively regulate CHS.

Engagement of CD47 inhibits the contact hypersensitivity response via the suppression of motility and B7 expression by Langerhans cells.

CD47 is a membrane-associated glycoprotein that suppresses the function of immune cells. We previously reported that Langerhans cells (LCs) express Src homology 2 domain-containing protein tyrosine phosphatase substrate 1 (SHPS-1), a ligand for CD47, which plays an important role in the regulation of their motility. In this study, we show that LCs also express CD47, and that ligation of CD47 with SHPS-1-Fc fusion protein in vivo diminishes the development of the contact hypersensitivity response. We further demonstrate that CD47 engagement affects immune functions of LCs. CD47 engagement in vivo significantly inhibits the emigration of LCs from the epidermis into draining lymph nodes following treatment with haptens and tumor necrosis factor-alpha. The emigration of dendritic cells from skin explants into the medium and the chemotaxis of murine XS52 dendritic cells were significantly reduced by treatment with SHPS-1-Fc or an anti-CD47 mAb. Under explant culture system, SHPS-1-Fc treatment suppressed the expression of CD80 and CD86 of LCs. These effects on LCs and contact hypersensitivity response of CD47 ligation were reversed by treatment with pertussis toxin. These results suggest that the ligation of CD47 inhibits the migration of LCs and the expression of B7 costimulatory molecules, which results in inhibition of the contact hypersensitivity response.

Responsiveness to autologous sweat and serum in cholinergic urticaria classifies its clinical subtypes.

BACKGROUND: It has been reported that patients with cholinergic urticaria have a type 1 allergy to autologous sweat; however, the pathogenesis of that disorder has not been fully elucidated. OBJECTIVE: We investigated the responsiveness to autologous sweat and serum in patients with cholinergic urticaria in relation to their clinical characteristics. We further classified the clinical subtypes that are clearly characterized by responsiveness to in vivo and in vitro tests as well as their clinical features. METHODS: Intradermal tests with autologous sweat and serum were performed in 18 patients with cholinergic urticaria. Histamine release from peripheral blood basophils induced by autologous sweat was measured. RESULTS: Eleven of 17 patients with cholinergic urticaria showed positive reactions in skin tests with their own diluted sweat. Substantial amounts of sweat-induced histamine release from autologous basophils were observed in 10 of 17 patients. Eight of 15 patients with cholinergic urticaria showed positive reactions in the autologous serum skin tests. All 6 patients who developed satellite wheals after the acetylcholine test showed hypersensitivity to sweat. Further, patients whose eruptions were coincident with hair follicles showed positive responses to the skin test with autologous serum, whereas patients whose eruptions were not coincident with hair follicles did not. CONCLUSION: On the basis of these findings, we propose that cholinergic urticaria should be classified into 2 distinct subtypes. The first (nonfollicular) subtype shows strong positive reactions to autologous sweat and negative reactions to autologous serum. The second (follicular) subtype shows weak reactions to autologous sweat and positive reactions to autologous serum.

Src homology 2 domain-containing protein tyrosine phosphatase substrate 1 regulates the migration of Langerhans cells from the epidermis to draining lymph nodes.

Src homology 2 domain-containing protein tyrosine phosphatase substrate 1 (SHPS-1) is a member of the signal regulatory protein family in which the extracellular region interacts with its ligand, CD47. Recent studies have demonstrated that SHPS-1 plays an important role in cell migration and cell adhesion. We demonstrate in this study, using immunohistochemical and flow cytometric analyses, that murine Langerhans cells (LCs) express SHPS-1. Treatment of mice ears with 2,4-dinitro-1-fluorobenzene significantly reduced the number of epidermal LCs, and that reduction could be reversed by pretreatment with mAb to SHPS-1 or the CD47-Fc fusion protein. Treatment with the SHPS-1 mAb in vivo reduced the number of FITC-bearing cells in the lesional lymph nodes after the application of FITC to the skin. The SHPS-1 mAb inhibited the in vivo TNF-alpha-induced migration of LCs. The emigration of dendritic cells expressing I-A(b+) from skin explants to the medium was also reduced by the SHPS-1 mAb. We further demonstrate that the chemotaxis of a murine dendritic cell line, XS52, by macrophage inflammatory protein-3beta was significantly inhibited by treatment with the SHPS-1 mAb or CD47-Fc recombinant protein. Finally, we show that migration of LCs was attenuated in mutant mice that lack the intracellular domain of SHPS-1. These observations show that the ligation of SHPS-1 with the SHPS-1 mAb or with CD47-Fc abrogates the migration of LCs in vivo and in vitro, which suggests that the SHPS-1-CD47 interaction may negatively regulate LC migration.