Sebocytes differentially express and secrete adipokines.

In addition to producing sebum, sebocytes link lipid metabolism with inflammation at a cellular level and hence, greatly resemble adipocytes. However, so far no analysis was performed to identify and characterize the adipocyte-associated inflammatory proteins, the members of the adipokine family in sebocytes. Therefore, we determined the expression profile of adipokines [adiponectin, interleukin (IL) 6, resistin, leptin, serpin E1, visfatin, apelin, chemerin, retinol-binding protein 4 (RBP4) and monocyte chemoattractant protein 1 (MCP1)] in sebaceous glands of healthy and various disease-affected (acne, rosacea, melanoma and psoriasis) skin samples. Sebaceous glands in all examined samples expressed adiponectin, IL6, resistin, leptin, serpin E1 and visfatin, but not apelin, chemerin, RBP4 and MCP1. Confirming the presence of the detected adipokines in the human SZ95 sebaceous gland cell line we further characterized their expression and secretion patterns under different stimuli mimicking bacterial invasion [by using Toll-like receptor (TLR)2 and 4 activators], or by 13-cis retinoic acid (13CRA; also known as isotretinoin), a key anti-acne agent. With the exception of resistin, the expression of all of the detected adipokines (adiponectin, IL6, leptin, serpin E1 and visfatin) could be further regulated at the level of gene expression, showing a close correlation with the secreted protein levels. Besides providing further evidence on similarities between adipocytes and sebocytes, our results strongly suggest that sebocytes are not simply targets of inflammation but may exhibit initiatory and modulatory roles in the inflammatory processes of the skin through the expression and secretion of adipokines.

Nijmegen breakage syndrome complicated with primary cutaneous tuberculosis.

Nijmegen breakage syndrome (NBS) is a rare autosomal recessive chromosomal instability syndrome characterized by severe immunodeficiency, growth retardation, microcephaly, a distinct facial appearance, and a high predisposition to lymphoid malignancy. We report a 7-year-old white girl with NBS associated with cutaneous tuberculosis. The patient presented with multiple red-brown, centrally scaring plaques on the leg and had neither pulmonary nor systemic manifestation of tuberculosis. Polymerase chain reaction testing using Mycobacterium genus- and Mycobacterium tuberculosis species-specific primers confirmed the clinical diagnosis of cutaneous tuberculosis. This is the first report describing the simultaneous presentation of NBS and cutaneous tuberculosis.

[Report on erythroderma and scabies infection in connection with two cases of scabies norvegica]. / Az erythrodermáról és rühatkafertozésrol scabies norvegica két esete kapcsán.

Erythroderma is an inflammation of almost the whole surface of the skin, characterized by erythema, skin infiltration and desquamation. Despite the etiological factors, the generalized inflammation of a large body surface can lead to a life-threatening condition in itself. Parasite infection lies rarely in the background of erythroderma. The Sarcoptes scabiei var. hominis belonging to the mite family is the cause of scabies disease. While the prevalence of "classic" scabies is high world-wide, the more severe and more dangerous form - scabies norvegica - is only seldom observed. Diagnosis and treatment is highly important from an epidemiological aspect. The authors discuss the differential diagnostic problems and epidemiological significance of scabies infection and erythroderma using two cases.

[Jellyfish sting. A case report]. / Medúzacsípésrol egy eset kapcsán.

Jellyfish bites in Hungary are rare. Yet, from a differential diagnostic point of view this epizoonozis might gain importance given the ever-growing popularity of seaside tourism. A 10 year old female patient was stung by a jellyfish while sea-bathing in the Adriatic in the summer of 2005. A couple of minutes after the bite urticaria were formed in the contacted area accompanied by a burning and sore sensation. In a few hours the above lesions turned livid and the patient developed low-grade fever and general discomfort. In acute therapy she received thorough rinse with vinegar, antibiotic ointment and systemic calcium. General symptoms regressed within 24 hours and dermatological symptoms improved progressively. Finally, the patient grew symptomless in 4 weeks altogether due to general antihistamine and local antibiotic therapy. 3 months later the patient presented again with hyperaemic papules and an increasing itching and burning sensation in the previously jellyfish-contacted area. Histopathology showed vascular involvement and eosinophilic infiltration. The inflammatory symptoms gradually diminished to locally applied steroids in an occlusive bandage leaving behind hypopigmentation. Although bare-skin contact with the different poisonous jellyfish species usually do lead to the forming of dermatological symptoms, vascular involvement developed months after the encounter in the exposure site has seldom been published. The article covers the main potential symptoms of jellyfish stings--both local and general--going into details about the possible dermatological differential diagnoses. Furthermore, the most venomous jellyfish species, their geographical habitats, do's and don't-s of first aid, therapy and prevention are being briefly discussed by the authors.

Activation of Notch1 signaling is required for beta-catenin-mediated human primary melanoma progression.

Notch is a highly conserved transmembrane receptor that determines cell fate. Notch signaling denotes cleavage of the Notch intracellular domain, its translocation to the nucleus, and subsequent activation of target gene transcription. Involvement of Notch signaling in several cancers is well known, but its role in melanoma remains poorly characterized. Here we show that the Notch1 pathway is activated in human melanoma. Blocking Notch signaling suppressed whereas constitutive activation of the Notch1 pathway enhanced primary melanoma cell growth both in vitro and in vivo yet had little effect on metastatic melanoma cells. Activation of Notch1 signaling enabled primary melanoma cells to gain metastatic capability. Furthermore, the oncogenic effect of Notch1 on primary melanoma cells was mediated by beta-catenin, which was upregulated following Notch1 activation. Inhibiting beta-catenin expression reversed Notch1-enhanced tumor growth and metastasis. Our data therefore suggest a beta-catenin-dependent, stage-specific role for Notch1 signaling in promoting the progression of primary melanoma.