No abstract available.
Child* ; Diphtheria-Tetanus-Pertussis Vaccine* ; Humans ; Infant*

No abstract available.
Decompression* ; Facial Nerve* ; Melkersson-Rosenthal Syndrome*

No abstract available.
Paranasal Sinuses*

No abstract available.
Child* ; Humans

No abstract available.
Embryonic Structures ; Fetus ; Humans* ; Kidney*

The formation, maintenance, and regeneration of bone is a complex precess involving the interactions of many cellular elements with systemic and local regulators. TGF-β is one of growth factors that play an important role in the formation and remodeling of bone. In vitro studies have suggested that TGF-β regulates chondrogenesis and possibly osteogenesis by affecting replication, gene expression, and structural protein synthesis in bone formation. We investigated the effect of TGF-β1 upon fracture callus formation and maturation in mature rate. Closed femoral shaft fracture was made consistently by three point stress technique after percutaneous intramedullary nailing. TGF-β1 was injected subperiosteally at the fracture site daily for 2 weeks. We examined the effect of TGF-β1 on the fracture healing process with the radiographic, densitometric, histologic, and immunohistochemical methods. The following results were obtained. 1. Radiographic examination demonstrated that TGF-β1 injection group appeared to have more abundant callus formation and earlier callus maturation as compared to the control group. 2. Bone densitometric examination revealed that TGF-β1 injection group had higher bone mineral density and content that the control group. 3. Thermographic examination revealed that TGF-β1 injection group had higher local temperature at the injection area than the control group. 4. Histologic examination suggested that TGF-β1 stimulates and accelerates fracture callus formation and endochondral bone formation. 5. Immunohistochemical examination revealed that chondrocytes at the fracture site in the TGF-β1 injection group seemed to produce type I collagen.
Bone Density ; Bony Callus ; Chondrocytes ; Chondrogenesis ; Collagen Type I ; Fracture Fixation, Intramedullary ; Fracture Healing ; Gene Expression ; In Vitro Techniques ; Intercellular Signaling Peptides and Proteins ; Osteogenesis ; Regeneration

No abstract available.
Cochlear Implants*

No abstract available.
Acute Kidney Injury* ; Carbon Monoxide* ; Carbon* ; Rhabdomyolysis*

To evaluate the possible therapeutic effects of growth hormone and vitamin C on multiorgan failure, a rat model was developed for LPS-induced sepsis. Using this model, the effects of growth hormone and vitamin C on tissue damages, catalase and i-NOS activities, and MDA levels were examined in the lung and liver. The level of TNF-in plasm was also examined. Male, Sprague-Dawley rats were injected with LPS intraperitoneally then divided into 3 groups : positive controls injected with LPS only, the ones injected with growth hormone or vitamin C immediately after the LPS injections. The lung and the liver were then isolated, blood samples were collected at 24 or 48 hours after the LPS injection, then examined for histopathological and biochemical changes. The results obtained were as follows. 1. LPS induced sinusoid vasodilation and mild destruction of lobular structure in the liver. In the lung, alveolar structure appeared to be thickened and interstitial edema was observed. The levels of MDA in the liver and the lung was increased by LPS, while the activity of catalase was decreased. The activity of i-NOS of those tissues was also increased, which was more pronounced at 24 hr. The level of TNF-in plasm was increased by LPS 2. In the lung, vitamin C suppressed lymphocyte and neutrophil infiltration, alveolar wall thickening and interstitial edema. In the liver, vitamin C protected against the destruction of the lobular structure. The activity of catalase reduced by LPS was reversed partly by vitamin C. The activity of i-NOS enhanced by LPS was also reversed by vitamin C. The level of TNF-in plasm reduced in some animals by vitamin C, which however was not significant statistically (P<0.05). 3. Growth hormone showed similar protective effects against inflammation and damages in the liver and lung tissues. Growth hormone reversed partly the LPS effects on the level of MDA, the activity of catalase and i-NOS induction in the liver and the lung. Growth hormone reduced plasma level of TNF-alpha substantially, which contrasted from vitamin C. Besides this, overall protective effects of growth hormone against LPS-induced experimental sepsis were similar to those of vitamin C. From this results, the mechanism of growth hormone on suppression of LPS-induced tissue damage might be associated with production of antioxidative enzyme and suppression of plasma TNF level.
Animals ; Ascorbic Acid ; Catalase ; Edema ; Growth Hormone ; Human Growth Hormone* ; Humans* ; Inflammation ; Liver ; Lung ; Lymphocytes ; Male ; Models, Animal* ; Neutrophil Infiltration ; Plasma ; Rats* ; Rats, Sprague-Dawley ; Sepsis* ; Tumor Necrosis Factor-alpha ; Vasodilation

No abstract available.
Nephrotic Syndrome*