The etiology of Behcet's disease has been proposed as being a viral, bacterial, genetic and immunological disorder. After Hulusi Behcet's viral etiological hypothesis, many investigators have tried to confirm this. Scrapings and fluids from patients were applied to subculture in chorioallantoic membranes of fertilized eggs as well as in mice and rabbits by direct intracerebral injection. Since the 1980s, in situ hybridization, blotting, and polymerase chain reaction has also been applied to identify the herpes simplex virus DNA and RNA in patients. Animal models were developed based on environmental pollutants, bacterial and human heat shock protein derived peptides and virus injection. Using these animal models separately and/or concurrently, allows for a more effective investigation into Behcet's disease.
Amino Acid Sequence ; Animal ; Behcet's Syndrome/etiology* ; Disease Models, Animal* ; Herpes Simplex/complications* ; Human ; Mice ; Molecular Sequence Data ; Rabbits

BACKGROUND: Keloids are characterized by excessive collagen deposition in the dermis, in which transforming growth factor β (TGF-β)/Smad signaling plays an important role. Low-level light therapy (LLLT) is reported as effective in preventing keloids in clinical reports, recently. To date, studies investigating the effect of LLLT on keloid fibroblasts are extremely rare. OBJECTIVE: We investigated the effect of LLLT with blue (410 nm), red (630 nm), and infrared (830 nm) light on the collagen synthesis in keloid fibroblasts. METHODS: Keloid fibroblasts were isolated from keloid-revision surgery samples and irradiated using 410-, 630-, 830-nm light emitting diode twice, with a 24-hour interval at 10 J/cm². After irradiation, cells were incubated for 24 and 48 hours and real-time quantitative reverse transcription polymerase chain reaction was performed. Western blot analysis was also performed in 48 hours after last irradiation. The genes and proteins of collagen type I, TGF-β1, Smad3, and Smad7 were analyzed. RESULTS: We observed no statistically significant change in the viability of keloid fibroblasts after irradiation. Collagen type I was the only gene whose expression significantly decreased after irradiation at 410 nm when compared to the non-irradiated control. Western blot analysis showed that LLLT at 410 nm lowered the protein levels of collagen type I compared to the control. CONCLUSION: LLLT at 410 nm decreased the expression of collagen type I in keloid fibroblasts and might be effective in preventing keloid formation in their initial stage.
Blotting, Western ; Collagen Type I ; Collagen* ; Dermis ; Fibroblasts* ; Humans* ; In Vitro Techniques* ; Keloid* ; Low-Level Light Therapy* ; Polymerase Chain Reaction ; Reverse Transcription ; Transforming Growth Factors

BACKGROUND: Progressive macular hypomelanosis, a disease of uncertain etiology, was first described by Guillet et al. in 1988. It is characterized by asymptomatic hypopigmented macules and patches that appear on the trunk and upper extremities. It is a relatively recently described disorder and more case reports are needed. OBJECTIVE: The purpose of the study was to document the clinicopathologic and ultrastructural features of progressive macular hypomelanosis in Korean patients. METHODS: Patients who presented to our hospital and were diagnosed with progressive macular hypomelanosis from July 2009 to June 2014 were enrolled in this study. Skin scrapings were taken for fungal tests, and skin biopsy specimens from lesional and normal skin were obtained. Sections of the skin biopsies were stained with hematoxylin and eosin, Brown and Brenn Gram stain, and Fontana-Masson stain, and they were incubated with a panel of immunohistochemical reagents used to identify melanocytes, namely, gp-100, melan-A, and microphthalmia-associated transcription factor. The tissues from two patients were also examined using electron microscopy. RESULTS: Over the course of 5 years, 16 patients presented with ill-defined hypopigmented macules on their trunks and upper extremities. The mean age of the patients was 28.4+/-9.0 years and the male to female ratio was about 1 : 4. Histopathologically, lesional skin showed a reduced level of pigmentation, while the number of melanocytes was preserved. None of the patients showed bacterial colonization of the pilosebaceous units. Electron microscopy demonstrated smaller and less melanized melanosomes in the lesional keratinocytes. CONCLUSION: Progressive macular hypomelanosis is a hypopigmentary disorder that is characterized by a loss of melanosomes without damage to the melanocytes. Although there are several reports that describe a possible relationship between Propionibacterium acnes and progressive macular hypomelanosis, it remains unclear.
Biopsy ; Colon ; Eosine Yellowish-(YS) ; Female ; Hematoxylin ; Humans ; Hypopigmentation* ; Indicators and Reagents ; Keratinocytes ; Korea ; Male ; MART-1 Antigen ; Melanocytes ; Melanosomes ; Microphthalmia-Associated Transcription Factor ; Microscopy, Electron ; Pigmentation ; Propionibacterium acnes ; Skin ; Upper Extremity

OBJECTIVES: We examined the patterns of cell death induced by the 6-hydroxydopamine, a selective dopaminergic toxin that used to produce Parkinson's disease model. METHOD: Neocortices from 14- or 15-day-old fetal mice for neuron-glia co-cultures were used for this experiments. RESULTS: Cortical cell cultures exposed to 10-100 microM 6-hydroxydopamine for 24 hr under-went neuronal death without injuring glia. The degenerating neurons showed hallmark of apoptosis featuring cell body shrinkage, nuclear chromatin condensation and aggregation, nuclear membrane disintegration with intact plasma membrane, and prominent internucle- osomal DNA fragmentation. Neither the glutamate antagonists (10 microM MK-801 and 50 microM CNQX) nor antioxidants (trolox, 100 microM, N-acetyl-cysteine, 100 microM) prevented the 6-OHDA induced neuronal injury. The death was attenuated by addition of two different anti-apoptotic agents, 1 microgram/ml cycloheximide and caspase inhibitor (100 microM zVAD-fmk). CONCLUSION: These features suggest that 6-OHDA induced apoptotic type of neuronal death in cortical neuronal culture. Considering the protective effect of caspase inhibitors, a mechanism involving caspase cascade rather than oxidative stress is responsible for the 6-OHDA-induced neuronal apoptosis. In addition, our results showed that 6-OHDA-induced apoptosis is not confined to dopaminergic neurons and the primary cortical culture system so this system is suitable for the study of 6-OHDA-induced neuronal apoptosis.
Animals ; Antioxidants ; Apoptosis* ; Caspase Inhibitors ; Cell Culture Techniques* ; Cell Death ; Cell Membrane ; Chromatin ; Coculture Techniques ; Cycloheximide ; Dizocilpine Maleate ; DNA Fragmentation ; Dopaminergic Neurons ; Excitatory Amino Acid Antagonists ; Mice* ; Neocortex ; Neuroglia ; Neurons* ; Nuclear Envelope ; Oxidative Stress ; Oxidopamine* ; Parkinson Disease