RESUMO
A 70-year-old male with a history of diabetes mellitus, hypertension, and coronary stent insertion visited our hospital 7 days after biting his lower lip. Swelling and inflammation had worsened despite debridement and antibiotic treatment. On the 8th hospital day, fungal infection with Candida albicans and superimposed bacterial infection with Klebsiella pneumoniae were found on tissue culture. Extensive necrosis resulted in a defect of approximately 3/4 of the entire lower lip and a full-layer skin defect from the vermilion to the gingivobuccal sulcus at the right corner of the mouth. To correct drooling, incomplete lip sealing, and trismus, staged reconstruction was performed with consideration of cosmetic and functional features. The treatment process using staged reconstruction and antifungal treatment for an extensive lower lip defect caused by fungal stomatitis is described.
RESUMO
Vascular dementia (VaD) is the second most common cause of dementia. It occurs when the cerebral blood supply is reduced by disarrangement of the circulatory system. Environmental enrichment (EE) has been associated with cognitive improvement, motor function recovery, and anxiety relief with respect to various neurodegenerative diseases and emotional stress models. The purpose of this study was to determine whether long-term EE influenced cognitive impairment in a rat model of chronic hypoperfusion induced by permanent occlusion of bilateral common carotid arteries (BCCAo). The Y-maze and Morris water maze tests were performed to evaluate the rats' cognitive functions. Also, the protein expression of brain-derived neurotrophic factor (BDNF), phosphorylated cAMP-calcium response element binding protein (pCREB), and vascular endothelial growth factor (VEGF) were confirmed by Western blot. The microvessels and angiogenesis-associated proteins in the hippocampal region were investigated using immunohistochemistry. The VaD + EE group showed significantly better cognitive functions than the VaD group in both the Y-maze and MWM tests. In addition, the VaD + EE group showed significantly increased expression of BDNF, pCREB, and VEGF in the hippocampus compared to the VaD group. Rats in the VaD + EE group also had increased length of microvessels and VEGF expression in the hippocampus. These results suggest that long-term EE exerts neuroprotective effects against cognitive impairment induced by chronic cerebral hypoperfusion through the enhancement of BDNF, pCREB, and VEGF expression and indicate that EE may be a good nursing intervention in vascular dementia patients.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Transtornos Cognitivos/patologia , Modelos Animais de Doenças , Aprendizagem em Labirinto , Transtornos da Memória , Condicionamento Físico Animal/métodos , Animais , Meio Ambiente , Feminino , Hipocampo , Masculino , Ratos , Ratos WistarRESUMO
PURPOSE: This study was done to identify whether pre-conditioning exercise has neuroprotective effects against cerebral ischemia, through enhance brain microvascular integrity. METHODS: Adult male Sprague-Dawley rats were randomly divided into four groups: 1) Normal (n=10); 2) Exercise (n=10); 3) Middle cerebral artery occlusion (MCAo), n=10); 4) Exercise+MCAo (n=10). Both exercise groups ran on a treadmill at a speed of 15 m/min, 30 min/day for 4 weeks, then, MCAo was performed for 90 min. Brain infarction was measured by Nissl staining. Examination of the remaining neuronal cell after MCAo, and microvascular protein expression on the motor cortex, showed the expression of Neuronal Nuclei (NeuN), Vascular endothelial growth factor (VEGF) & laminin. RESULTS: After 48 hr of MCAo, the infarct volume was significantly reduced in the Ex+MCAo group (15.6±2.7%) compared to the MCAo group (44.9±3.8%) (p<.05), and many neuronal cells were detected in the Ex+MCAo group (70.8±3.9%) compared to the MCAo group (43.4±5.1%) (p<.05). The immunoreactivity of laminin, as a marker of microvessels and Vascular endothelial growth factor (VEGF) were intensively increased in the Ex+MCAo group compared to the MCAo group. CONCLUSION: These findings suggest that the neuroprotective effects of exercise pre-conditioning reduce ischemic brain injury through strengthening the microvascular integrity after cerebral ischemia.