Successful hyaluronic acid filler injection in a chronic myeloid leukemia patient taking imatinib mesylate.

Dermal fillers are highly favored around the globe as minimally invasive or nonsurgical procedures. Imatinib mesylate is the first-line treatment for patients diagnosed with chronic myeloid leukemia. However, some studies describe that imatinib mesylate may increase the tendency of skin fragility which can lead to easy bruising and hyperpigmentation after invasive skin procedures. Yet, to our knowledge, no studies have described any successful dermal filler injection performed on patients who are under imatinib mesylate treatment. Hence, we present a case successfully treated with hyaluronic acid filler injection on a patient under imatinib mesylate treatment. We carefully propose that hyaluronic acid filler can be an effective means of rejuvenation and cosmetic enhancement for those under imatinib mesylate treatment.

Varicella-zoster virus as a possible cause of pityriasis lichenoides et varioliformis acuta.

The etiologic agents for pityriasis lichenoides et varioliformis acuta (PLEVA) are largely unknown, although it has been suggested that foreign antigens such as infectious agents are the pathogenic mechanism. We present a case suggesting a possible relationship between varicella-zoster virus and PLEVA.

Chondroid syringoma with marked calcification.

Chondroid syringoma is an uncommon benign neoplasm in the skin. It is composed of epithelial and myoepithelial cells embedded in a matrix with varying amounts of mucoid and cartilaginous material. Chondroid syringoma is classified into 2 types, the apocine type and the eccrine type. Several cases of the eccrine type chondroid syringoma with ossification and calcification have been reported, but the apocrine type chondroid syringoma with calcification has not been reported. In this report, we describe a case of apocrine type chondroid syringoma with calcification.

Coexistence of congenital linear porokeratosis and disseminated superficial porokeratosis.

The coexistence of two or more forms of porokeratosis in a single individual is rarely reported. We report here on a patient exhibiting the coexistence of congenital linear porokeratosis and disseminated superficial porokeratosis. To our knowledge, this entity has been previously reported only once.

Roxatidine suppresses inflammatory responses via inhibition of NF-κB and p38 MAPK activation in LPS-induced RAW 264.7 macrophages.

Roxatidine is a novel, specific, competitive H(2) -receptor antagonist that is used to treat gastric and duodenal ulcers, and which is known to suppress the growth of several tumors by reducing vascular endothelial growth factor (VEGF) expression. Nevertheless, it remains unclear whether roxatidine has anti-inflammatory effects. In this study, we the authors investigated the anti-inflammatory effect of roxatidine in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. It was found that roxatidine dose-dependently inhibited the productions of prostaglandin E(2) (PGE(2)), nitric oxide (NO), and histamine, and the protein and mRNA expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and histidine decarboxylase (HDC). In addition, roxatidine reduced the productions and expressions of VEGF-1 and pro-inflammatory cytokines, including those of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6). Electrophoretic mobility shift assays (EMSA) and reporter gene assays revealed that treatment with roxatidine attenuated the LPS-induced DNA-binding and transcriptional activity of nuclear factor kappa B (NF-κB). In addition, it was found that pretreatment with roxatidine significantly inhibited the nuclear translocations of the p65 and p50 subunits of NF-κB, and these inhibitions were not found to be associated with decreases in the phosphorylation or degradation of inhibitory kappa B-α (IκBα). Furthermore, roxatidine suppressed the phosphorylation of p38 MAP kinase, but not of IκB kinase-α/ß (IKKα/ß), c-Jun NH(2) -terminal kinase (JNK), or extracellular signal-regulated kinase (ERK). Taken together, these results indicate that the anti-inflammatory properties of roxatidine in LPS-treated RAW 264.7 macrophages are mediated by the inhibition of NF-κB transcriptional activity and the p38 MAP kinase pathway.

Chronic mild stress decreases survival, but not proliferation, of new-born cells in adult rat hippocampus.

New-born cells continue to proliferate and survive to become mature granule cells in adult rat hippocampus. Although this process, known as neurogenesis, is inhibited by acute stress, it is not clear whether chronic stress affects neurogenesis. To determine whether chronic mild stress (CMS) influences neurogenesis in the adult rat hippocampus, male Sprague-Dawley rats were exposed to CMS and administered bromodeoxyuridine (BrdU) before or after CMS to observe the survival/differentiation or proliferation of new-born cells, respectively. In addition, we measured brain-derived neurotrophic factor (BDNF) mRNA in the granule cell layer (GCL) of the hippocampus, because BDNF is known to play an important role in the survival of new-born cells. CMS significantly decreased the survival of new-born cells in the GCL, but did not influence the proliferation or differentiation of new-born cells. CMS did not affect the proliferation and survival of new-born cells in the hilus. In addition, CMS did not change BDNF mRNA levels in the GCL. These results demonstrate that CMS reduces the survival of new-born cells but not of their proliferation, suggesting that repeated mild stress could influence a part of neurogenesis, but not the whole part of neurogenesis. These results raise the possibility that the survival of new-born cells may be suppressed in the presence of normal BDNF mRNA levels in GCL.

Chemopreventive effects of standardized ethanol extract from the aerial parts of Artemisia princeps Pampanini cv. Sajabal via NF-κB inactivation on colitis-associated colon tumorigenesis in mice.

Chronic inflammation is an underlying risk factor of colon cancer, and NF-κB plays a critical role in the development of inflammation-associated colon cancer in an AOM/DSS mouse model. The aim of this study was to determine whether the standardized ethanol extract obtained from the aerial parts of Artemisia princeps Pampanini cv. Sajabal (EAPP) is effective at preventing inflammation-associated colon cancer, and if so, to identify the signaling pathways involved. In the present study, protective efficacy of EAPP on tumor formation and the infiltrations of monocytes and macrophages in colons of an AOM/DSS mouse model were evaluated. It was found that colitis and tumor burdens showed statistically meaningful improvements after EAPP administration. Furthermore, these improvements were accompanied by a reduction in NF-κB activity and in the levels of NF-κB-dependent pro-survival proteins, that is, survivin, cFLIP, XIAP, and Bcl-2. In vitro, EAPP significantly reduced NF-κB activation and the levels of IL-1ß and IL-8 mRNA and pro-survival proteins in HT-29 and HCT-116 colon cancer cells. Furthermore, EAPP caused caspase-dependent apoptosis. Based on these results, the authors suggest EAPP suppresses inflammatory responses and induces apoptosis partly via NF-κB inactivation, and that EAPP could be useful for the prevention of colitis-associated tumorigenesis.

Anti-inflammatory effect of a standardized triterpenoid-rich fraction isolated from Rubus coreanus on dextran sodium sulfate-induced acute colitis in mice and LPS-induced macrophages.

ETHNOPHARMACOLOGICAL RELEVANCE: Rubus coreanus Miquel (Rosaceae), the Korean black raspberry, has traditionally been used to treat inflammatory diseases including diarrhea, asthma, stomach ailment, and cancer. Although previous studies showed that the 19α-hydroxyursane-type triterpenoids isolated from Rubus coreanus exerted anti-inflammatory activities, their effects on ulcerative colitis and mode of action have not been explored. This study was designed to assess the anti-inflammatory effects and the molecular mechanisms involving19α-hydroxyursane-type triterpenoid-rich fraction from Rubus coreanus (TFRC) on a mice model of colitis and lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. MATERIALS AND METHODS: Experimental colitis was induced by DSS for 7 days in ICR mice. Disease activity indices (DAI) took into account body weight, stool consistency, and gross bleeding. Histological changes and macrophage accumulation were observed by immunohistochemical analysis. Pro-inflammatory markers were determined using immunoassays, RT-PCR, and real time PCR. Signaling pathway involving nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) activation was determined by luciferase assay and Western blotting. RESULTS: In DSS-induced colitis mice, TFRC improved DAIs and pathological characteristics including colon shortening and colonic epithelium injury. TFRC suppressed tissue levels of pro-inflammatory cytokines and reduced macrophage infiltration into colonic tissues. In LPS-induced RAW 264.7 macrophages, TFRC inhibited the production of NO, PGE2, and pro-inflammatory cytokines by down-regulating the activation of NF-κB and p38 MAPK signaling. CONCLUSION: The study demonstrates that TFRC has potent anti-inflammatory effects on DSS-induced colonic injury and LPS-induced macrophage activation, and supports its possible therapeutic and preventive roles in colitis.

Effects of Korean red ginseng extract on the prevention of atopic dermatitis and its mechanism on early lesions in a murine model.

ETHNOPHARMACOLOGICAL RELEVANCE: Korean red ginseng (KRG) has been shown to possess various biological activities including anti-inflammatory properties. AIM OF THE STUDY: We aimed to investigate the effects and mechanism of KRG on the prevention of atopic dermatitis (AD) using a mouse model. MATERIALS AND METHODS: The effect of KRG in trinitrochlorobenzene (TNCB)-treated NC/Nga mice was assessed by measuring ear thickness, transepidermal water loss (TEWL), total serum IgE, histologic changes of lesional skin, mRNA and protein expression of thymic stromal lymphopoietin (TSLP) and tumor necrosis factor (TNF)-α, immunohistochemistry for tissue interleukin (IL)-4, IL-17, and interferon (IFN)-γ. RESULTS: KRG significantly reduced ear thickness. Oral administration of KRG significantly prevented the increase in TEWL induced by TNCB. The serum IgE level was significantly lower in the KRG group. Histologically, lymphocyte infiltration was markedly decreased by KRG. CD1a positive (CD1a+) cells were diminished by KRG. Immunohistochemically, KRG significantly suppressed the protein expression of TSLP and TNF-α. The mRNA expression of TSLP in the lesions was significantly reduced by KRG. These results demonstrate that oral administration of KRG may inhibit the development of AD-like skin lesions in NC/Nga mice by modifying TSLP, DCs, and at least in part, the Th2 response. CONCLUSION: KRG may be a potential therapeutic modality for the prevention of AD.

Progressive cribriform and zosteriform hyperpigmentation: a clinicopathologic study.

BACKGROUND: Progressive cribriform and zosteriform hyperpigmentation (PCZH) is a disorder of pigmentation. Although several cases of PCZH have been reported, no clinicopathologic studies of the condition have been published in the English-language literature. OBJECTIVES: The purpose of this study was to determine the clinical characteristics and histologic findings of PCZH. METHODS: Between 1999 and 2009, 30 patients were diagnosed with PCZH in our Department of Dermatology. Medical records, clinical photographs, and pathologic findings for each patient were retrospectively reviewed. RESULTS: The patients included 16 men and 14 women. The mean age at onset was 14.27 years. The trunk was the most common site of involvement. Microscopic examination showed an increased level of melanin pigment in the basal cell layer compared with adjacent normal skin, although no significant difference existed in the number of melanocytes. Pigmentary incontinence was observed in 13 of 30 cases. CONCLUSIONS: There was no significant difference in prevalence, age at onset, and duration of lesions between male and female patients with PCZH. The lesions corresponded to the lines of Blaschko and were localized rather than exhibiting diffuse patterns. A common feature of the histopathologic findings was higher melanin content in the lesions than in normal skin but with no significant difference in the number of melanocytes.

Type B pigmentary demarcation lines of pregnancy involving the anterior thighs and knees.

Pigmentary demarcation lines are abrupt transition lines between the areas of deeper pigmentation and the areas of lighter, normal pigmentation. Type B pigmentary demarcation lines involve the posterior medial portion of the lower extremities and are more commonly associated with pregnancy. We present a case of pigmentary demarcation lines of pregnancy with erythematous changes, involving both the anterior and posterior aspects of the lower extremities.

Arvelexin inhibits colonic inflammation by suppression of NF-κB activation in dextran sulfate sodium-induced mice and TNF-α-induced colonic epithelial cells.

Recently, we reported the anti-inflammatory effects of arvelexin isolated from Brassica rapa in macrophages. In the present study, the effects of arvelexin were investigated in a dextran sulfate sodium (DSS)-induced colitis mouse model and in a cellular model. In the DSS-induced colitis model, arvelexin significantly reduced the severity of colitis, as assessed by disease activity, colonic damage, neutrophil infiltration, and levels of colonic iNOS. Moreover, arvelexin inhibited the expressions of IL-8, IP-10, ICAM-1, and VCAM-1 in HT-29 colonic epithelial cells. Arvelexin also inhibited the TNF-α-induced adhesion of U937 monocytic cells to HT-29 cells. Furthermore, arvelexin reduced p65 NF-κB subunit translocation to the nucleus and IκBα degradation in the colonic tissues and in TNF-α-induced HT-29 cells. These results demonstrate that the ameliorative effects of arvelexin on colonic injury are mainly related to its ability to inhibit the inflammatory responses via NF-κB inactivation, and support its possible therapeutic role in colitis.

Polyphenon-60 displays a therapeutic effect on acne by suppression of TLR2 and IL-8 expression via down-regulating the ERK1/2 pathway.

Propionibacterium acnes (P. acnes) is a well-known acne-inducing factor which causes inflammatory skin lesions by enhancing cytokine production through toll-like receptor 2 (TLR2). Green tea extract catechin has been documented to possess anti-inflammatory effects. However, little is known about the mechanisms involved or any direct effect of green tea catechin on acne. The present study investigated the therapeutic effects and mechanism of polyphenon-60, also known as green tea catechin compound, on acne in vitro and in vivo. In a clinical study using topical polyphenon-60 treatment, acne patients showed symptomatic improvement with decrease in the number of comedos and pustules. To investigate the mechanism underlying the activity of polyphenon-60 in acne therapy, an in vitro study was performed. We found that polyphenon-60 reduced the levels of P. acnes-enhanced TLR2 and interleukin-8 (IL-8) in THP-1 cells, human monocyte cell line and human primary monocytes. Taken together, these data demonstrate that polyphenon-60 has a therapeutic effect on acne by suppressing inflammation, specifically by inhibiting TLR2 expression and IL-8 secretion via down-regulation of extracellular signal-regulated kinases 1/2 (ERK1/2) pathway and activator protein-1 (AP-1) pathway.

A case of reactive eccrine syringofibroadenoma.

Eccrine syringofibroadenoma is a rare adnexal tumor of eccrine ductal differentiation with variable clinical features. It manifests as either a solitary or multiple papules and nodules arranged in a symmetrical or linear pattern. The anatomical distribution is wide and includes the face, trunk, extremities, and rarely the nails. Histopathological findings show anastomosing cords and strands of uniform cuboidal cells surrounded by fibrovascular stroma. Herein, we report a case of reactive eccrine syringofibroadenoma which developed on the foot of a 37-year-old woman, after self-paring of tissue and subsequent infection and ulceration.

Systemic contact dermatitis from propolis ingestion.

Propolis, also known as bee glue, is a substance collected by worker bees and it is used as a material for constructing and maintaining their beehives. It has been used topically and orally by humans for its anti-inflammatory properties. However, the growing use of propolis has been paralleled by reports of allergic contact dermatitis as a reaction to the substance. Contact dermatitis with generalized cutaneous manifestations elicited by propolis ingestion has not been previously reported. Here we report on the first case of systemic contact dermatitis from propolis ingestion in a 36-year-old woman.