Ayako Futagami

Wound healing involves induction of cyclooxygenase-2 expression in rat skin.

Cyclooxygenase (COX), an enzyme essential for prostaglandin biosynthesis, has two isoforms, COX-1 and -2. We investigated temporal and spatial changes in localization of these two COX proteins and mRNAs after excisional injury in rat skin. We also quantified the expression of these proteins and studied the effects of a specific COX-2 inhibitor on healing. Immunohistochemistry and in situ hybridization respectively indicated that the COX-2 protein and mRNA were expressed mainly within the basal layer of the epidermis, peripheral cells in the outer root sheath of hair follicles, and fibroblast-like cells and capillaries near epidermal wound edges. Much less intense expression was observed in normal skin than in injured skin. Western analysis demonstrated marked induction of COX-2 protein beginning within 12 hours and peaking 3 days after injury. In contrast, localization of COX-1 protein and mRNA, as well as the amount of protein expression, showed no significant change during wound healing. Administration of the COX-2 inhibitor delayed re-epithelialization in the early phase of wound healing and also inhibited angiogenesis. Thus, COX-2 induction may be important in cutaneous wound healing.

Basal cell carcinoma arising on a chronic lymphedematous leg

We describe a case of an 82‐year‐old Japanese woman with basal cell carcinoma (BCC) on the leg with secondary chronic lymphedema due to treatment for uterine cancer. Sparse tumor nests with remarkable edema of the dermis in the nodule appeared to be influenced by the chronic lymphedema. However, it remains inconclusive whether or not the tumorigenesis of the BCC was associated with chronic lymphedema in this case.

A case of peripheral T-cell lymphoma unspecified involving subcutaneous tissue

A 36-year-old man presented with a 3-year-old red-brown plaque with subcutaneous nodules on his left thigh. Although a similar lesion was observed on his right thigh 3 years earlier, it spontaneously disappeared 1 year later. However, the lesion on the left thigh was growing larger. Histologically, the lesion showed a diffuse and dense infiltration of atypical lymphocytes extending from the superficial dermis to the subcutaneous tissue. Severe lobular panniculitis, composed of small- and medium-sized atypical lymphocytes and large normal histiocytes, was observed in the subcutaneous adipose tissue. Immunohistochemical studies revealed a post-thymic T-cell phenotype. A genetic analysis demonstrated a rearrangement of the T-cell receptor chain gene. The left skin lesion also gradually disappeared after skin biopsy without therapy, and he continues to be in remission.

A case of erythrodermic-CTCL.

There are some types of leukemia and lymphoma, especially T-cell types, that show skin infiltration and possibly cause erythroderma. Recently, the International Society for Cutaneous Lymphomas (ISC...

Follicular lymphoma presenting follicular papules in the skin: A case report

ularly shaped blood vessels proliferating mainly in the dermis, with an infiltrate of lymphocytes and eosinophils in the dermal stroma (Fig. 1b). A high-power view revealed the aberrant vessels lined by plump, epithelioid endothelial cells (Fig. 1c). The deep subcutaneous nodule consisted of a well-circumscribed but non-encapsulated proliferation of dilated blood vessels of various sizes (Fig. 1b). These proliferating blood vessels consisted of intermingled thick-walled and thin-walled vessels (Fig. 1d). Elastica van Gieson staining showed internal elastic lamina in very few vessels, indicating that most of the blood vessels were veins (Fig. 1e). An obvious arteriovenous shunt was not identified. These clinical and histopathological findings led to the diagnosis of angiolymphoid hyperplasia with eosinophilia (ALHE) associated with underlying arteriovenous hemangioma (AVH). The endothelial cells in ALHE were immunoreactive to hypoxia-inducible factor (HIF)-1a, and rarely in AVH (Figs 1f,g). No recurrence was seen during a 3-year follow up. Angiolymphoid hyperplasia with eosinophilia, also known as epithelioid hemangioma, is an uncommon benign vascular lesion with distinct clinicopathological characteristics. Its etiology and pathogenesis are still uncertain. There is considerable controversy whether ALHE is a reactive lesion or a true neoplasm. Olsen and Helwig found arteriovenous malformation (AVM) in 42% of ALHE, and regard AVM as a possible cause of ALHE. Other authors also reported cases associated with arteritis, thrombus and AVM, mentioning the causal relationship of arterial lesions to ALHE. Sun et al. postulated that local hypoxia may play a role in the pathogenesis of ALHE. Our patient had underlying AVH in combination with ALHE. AVH is a rare, benign, acquired vascular lesion of unknown pathogenesis. To our knowledge, AVH, which is a type of hemangioma, not malformation, has never been described as a comorbidity of ALHE. We hypothesized that our patient had local hypoxia due to underlying AVH and the hypoxic condition led to endothelial cell proliferation, causing ALHE. In this case, diffuse cytoplasmic and moderate nuclear immunoreactivity of the endothelial cells for HIF-1a was observed in ALHE. HIF-1 is an oxygen-dependent transcription factor, which plays a crucial role in the angiogenesis of tumors. If hypoxia occurs, the HIF-1a subunit becomes stable and interacts with co-activators to modulate its transcriptional activity. Overexpression of HIF-1a can lead to the production of various hypoxia-inducible mRNA, including the mRNA encoding vascular endothelial growth factor, platelet-derived growth factor B, erythropoietin, galectin-3, WT-1 protein and transforming growth factor-a, which are confirmed stimulators of endothelial cell proliferation. Hypoxia may also promote endothelial cell proliferation though the renin–angiotensin–aldosterone system. Coexistence of ALHE with underlying deep type AVH and the immunohistochemical results in our case favor the hypothesis that ALHE is a reactive lesion triggered by hypoxia.

Case of basal cell carcinoma with ductal differentiation.

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Tenosynovial Giant Cell Tumor Arising on the Scapular Region

Tenosynovial giant cell tumor (TSGCT) is a benign soft tissue tumor arising from the synovial membrane that composes the lining of joints, tendons and bursae. TSGCT is a common tumor occurring in the hands and fingers, and also consecutively in the knees, ankles, feet and hips. It is rarely found in the scapular region. To the best of our knowledge, only 2 cases arising on the upper back have been reported. This report presents the case of a 44-year-old Japanese female with a TSGCT arising on her right scapular region.

Folliculosebaceous cystic hamartoma associated with melanocytic nevus

Figure 1. Clinical findings. A dome-shaped nodule was observed on the right side of the nose. Dear Editor, Folliculosebaceous cystic hamartoma (FSCH), originally described by Kimura et al., is widely considered to consist of multiple tissue elements, including ectodermal and mesodermal components. In rare cases, FSCH is associated with other conditions, such as rosacea, nevus lipomatosus superficialis or portwine stain. In the present report, we describe a case of melanocytic nevus exhibiting features of FSCH. To the best of our knowledge, this is the first report describing a case in which the patient showed histopathological features of both FSCH and melanocytic nevus. A 64-year-old Japanese man visited an outpatient clinic run by the Department of Dermatology, Nippon Medical School. He complained of a nodule on the right side of his nose, which had been present since the past 3 years. Clinical examination revealed that this nodule was 1.0 cm in diameter, dome-shaped, elastic and hard (Fig. 1). Part of the lesion was grey (Fig. 1). Our clinical diagnosis was melanocytic nevus. The lesion was surgically removed under local anesthesia. Histological examination revealed a large, dilated, cystic structure lined by stratified squamous epithelium; the structure resembled the follicular infundibulum (Fig. 2). Multiple sebaceous lobules radiated from the periphery of the cystic structure. In some instances, sebaceous ducts were observed. The stroma surrounding the epithelial component of the cyst and the sebaceous lobules consisted of dense fibrous tissue with scattered adipocytes (Fig. 2). Clefts were present between this stroma and the surrounding altered stroma (Fig. 2). Additional clefts were observed between the altered stroma and the adjacent fibrous tissue (Fig. 2). Melanocytic nests, some of which contained abundant melanin granules in their cytoplasm, were observed throughout the

Efficiency of Dermoscopy for the Clinical Diagnosis of Skin Disease

Synapses are the site of connections between various nerve cells to interact, where neural information is processed through the mechanisms of synaptic transmission mediated by chemical messengers, including excitatory and inhibitory neurotransmitters. Whereas signals at excitatory synapses are mediated by the amino acid glutamate, inhibitory signals are mainly mediated by γ-aminobutyric acid (GABA). Exploring the mechanisms underlying the synaptic transmission and changes in its strength is, therefore, essential for our understanding of brain functions. The inhibitory synapse plays a critical role in controlling various functions of the brain. However, the mechanisms that regulate the strength of transmission at inhibitory synapses are poorly understood than those that regulate excitatory synapses. Therefore, I have been interested in the roles of neuromodulators on inhibitory GABAergic synapses in the cerebellum, whose basic neural circuits and synaptic mechanisms have been more thoroughly investigated than have those of other regions of the mammalian central nervous system. This knowledge base would allow results of experiments on cerebellar synapses to be interpreted more easily. Consequently, our studies have revealed that GABAergic synapses in the cerebellum are well modulated by different neuromodulators (monoamines and purines) liberated by different synaptic inputs converging on the same inhibitory synapses. (日本医科大学医学会雑誌 2009; 5: 152―158)