PURPOSE: Transforming growth factor (TGF)-beta1 reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of TGF-beta1 on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether TGF-beta1 has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. METHODS: Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with TGF-beta1 (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% O2). TGF-beta1 (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. RESULTS: In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL TGF-beta1-treated group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the TGF-beta1-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the TGF-beta1-treated group except NR2C. CONCLUSION: The administration of TGF-beta1 could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Animals ; Anoxia ; Astrocytes ; Brain ; Brain Injuries ; Incubators ; Ischemia ; N-Methylaspartate ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II ; Rats ; Receptors, N-Methyl-D-Aspartate ; Transforming Growth Factor beta1 ; Transforming Growth Factors

PURPOSE: Transforming growth factor (TGF)-beta1 reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of TGF-beta1 on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether TGF-beta1 has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. METHODS: Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with TGF-beta1 (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% O2). TGF-beta1 (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. RESULTS: In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL TGF-beta1-treated group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the TGF-beta1-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the TGF-beta1-treated group except NR2C. CONCLUSION: The administration of TGF-beta1 could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Animals ; Anoxia ; Astrocytes ; Brain ; Brain Injuries ; Incubators ; Ischemia ; N-Methylaspartate ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II ; Rats ; Receptors, N-Methyl-D-Aspartate ; Transforming Growth Factor beta1 ; Transforming Growth Factors

Necrotizing fasciitis has been recognized as a potentially lethal and rapidly progressing infection. Necrotizing fasciitis of head and neck area is rare but fatal disease that should be prompt diagnosis and recognition. If not promptly recognized and treated, infection can spread into the deep spaces of the neck and compromise the airway. It may also spread into the mediastimum producing life threatening sepsis. In this report, we describe the treatment of 4 cases of necrotizing fasciitis of head and neck area and discuss diagnosis, treatment, complication and consideration with review of literatures.
Anti-Bacterial Agents ; Diagnosis ; Fasciitis, Necrotizing* ; Head* ; Neck* ; Sepsis

PURPOSE: To compare the case of widespread maxillary osteomyelitis treated through different approach. METHOD: We report the two case of osteomyelitis. In a case, we had gradually removed the small amount of sequestrum for several times. In the other case, intended Le Fort I fracture was done to approach the lesion. RESULT: In the gradual sequestrectomy case, bone formations were found after 4 months. In the other case, after intended Le Fort I down fracture, sequestrectomy of Lt. maxilla was done with the labiobuccal alveolar bone preserved for the prosthodontic treatment.
Maxilla* ; Osteomyelitis* ; Prosthodontics

Chondroblastoma ; Curettage ; Epiphyses ; Granuloma, Giant Cell ; Recurrence ; S100 Proteins ; Temporal Bone