No abstract available.
Child* ; Hand* ; Humans ; Leiomyoma* ; Male*

No abstract available.
Child* ; Hand* ; Humans ; Leiomyoma* ; Male*

Free radicals are known as an important factor which may act on reperfusion injury after transient or permanent brain ischemia. Numerous studies about cytotoxic function of free radical have been done. Most of these studies demonstrate the function of free radical in reperfusion injury by using radical scavenger or antioxidant as inhibitor of radicals. We used a modification of Karnovsky's Mn2 /diaminobenzidine (DAB) technique to demonstrate intravascular free radicals following transient occlusion and reperfusion of one middle cerebral artery in Sprague-Dawley rats. The MCA was occluded for 2 hours using an intraluminal suture method. The reperfusion time after transient ischemia was 1 hour, 6 hours, and 24 hours, respectively. Animals were perfused transcardially with solution containing Mn2 and DAB. After DAB perfusion, the brains were removed promptly, sectioned in frozen, and stained with methylene blue for light microscopic examination. Upon light microscopic examination, free radicals were confined within intravascular lumen and the amount of deposits increased according to the duration of reperfusion. Upon electron microscopic examination, free radicals were located in nuclear membrane and membrane of mitochondria and RER, and demonstrated as electron dense deposits. In addition, cell processes of the neuron revealed an electron dense deposits beneath the inner side of the membrane. In conclusion, free radicals demonstrated in the reperfusion injury area indicate that free radical acts as an important cytotoxic factor. Intracellular localization of free radicals may explain the relationship between free radical and delayed neuronal injury.
Animals ; Brain Ischemia* ; Brain* ; Free Radicals* ; Ischemia ; Membranes ; Methylene Blue ; Middle Cerebral Artery ; Mitochondria ; Neurons ; Nuclear Envelope ; Perfusion ; Rats, Sprague-Dawley ; Reperfusion Injury* ; Reperfusion* ; Sutures

Gorham-Stout disease is a rare bone disorder that is characterized by angiomatous proliferation and results in destruction and resorption of the osseous matrix. It has variable presentations and a number of different sites may be affected, including the dermis, soft tissue, and viscera. The involved cutaneous and soft tissue lesions typically present with sponge-like, soft, brown or purple lesions. The clinical course is generally prolonged, with eventual stabilization of the affected bone; however, it is rarely fatal. There is no standard treatment defined for this disease, and variable therapies such as medical, surgical, and radiation therapy have been used. We report a case of 24-year-old man with Gorham disease who presented with progressive cutaneous lesions and severe lymphedema adjacent to the diseased bone.
Dermis ; Humans ; Lymphedema ; Osteolysis, Essential* ; Viscera ; Young Adult

BACKGROUND: Inducible nitric oxide synthase (iNOS) has been detected in a number of pathologic conditions in the central nervous system. This study was investigated the patterns of iNOS expression in the neuronal PC12 cell and the effects of nitric oxide on the apoptosis of PC12 cells. METHODS: The stimulating agents for induction of iNOS expression in PC12 cells were bacterial lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-), and interferon-gamma (IFN-). RESULTS: The expression iNOS mRNA and protein in PC12 cells stimulated with LPS/TNF-/IFN- were profoundly increased. The expression of iNOS mRNA arose at 6 hours, peaked at 12 hours, and declined to 48 hours after LPS/TNF-/ IFN- treatment. iNOS protein was increased up to 24 hours in LPS/TNF-/IFN- treated PC12 cells while the expression of nNOS was unaffected. Accumulation of NO derivatives in the culture media was markedly increased at least at up to 48 hours after LPS/TNF-/IFN- treatment. The induction of iNOS expression and NO production in differentiated PC12 cells was correlated with apoptotic cell death judged by transmission electron microscopy and DNA fragmentation from the results of the Terminal deoxynucleotidyl-transferase-mediated dUDP biotin nick end-labeling (TUNEL) method. After treatment with NOS inhibitor, N-monomethylarginine (NMMA), a profound decrease in NO production by LPS/TNF-/IFN- treated PC12 cells was noted. And the LPS/TNF-/IFN- induced apoptosis was prevented by the NMMA treatment. CONCLUSIONS: From the above results it is concluded that the expression of iNOS in differentiated PC12 cells is induced by the combined application of LPS, TNF-, and IFN-. And the apoptosis of cultured PC12 cells is mediated by iNOS-derived NO.
Animals ; Apoptosis* ; Biotin ; Cell Death ; Central Nervous System ; Culture Media ; DNA Fragmentation ; Interferon-gamma ; Microscopy, Electron, Transmission ; Necrosis* ; Neurons* ; Nitric Oxide Synthase Type II* ; Nitric Oxide* ; PC12 Cells* ; RNA, Messenger ; Tumor Necrosis Factor-alpha

A 21-year-old male with no any other diseases presented with fever, chills, and chest discomfort. A chest radiography scan and a transthoracic echocardiogram revealed a large amount of pericardial effusion. An H1N1 viral real-time PCR test confirmed the presence of H1N1 viral infection. Pericardiocentesis was performed to reduce symptoms, and oseltamivir (Tamiflu(TM)) was administered. His symptoms improved during the first 4 days, and there was no relapse of the pericardial effusion. The most common manifestation of influenza A infection is respiratory tract infection. Although a cardiovascular manifestation is possible, it is extremely rare. We have reported here a case of acute pericarditis with a large amount of pericardial effusion in a healthy adult infected with influenza A virus (H1N1, swine-origin).
Adult* ; Chills ; Fever ; Humans ; Influenza A virus ; Influenza A Virus, H1N1 Subtype ; Influenza, Human* ; Male ; Oseltamivir ; Pericardial Effusion* ; Pericardiocentesis ; Pericarditis* ; Radiography ; Real-Time Polymerase Chain Reaction ; Recurrence ; Respiratory Tract Infections ; Swine* ; Thorax ; Young Adult