Luteolin Suppresses Inflammatory Mediator Expression by Blocking the Akt/NFκB Pathway in Acute Lung Injury Induced by Lipopolysaccharide in Mice

Acute lung injury (ALI), instilled by lipopolysaccharide (LPS), is a severe illness with excessive mortality and has no specific treatment strategy. Luteolin is an anti-inflammatory flavonoid and widely distributed in the plants. Pretreatment with luteolin inhibited LPS-induced histological changes of ALI and lung tissue edema. In addition, LPS-induced inflammatory responses, including increased vascular permeability, tumor necrosis factor (TNF)-α and interleukin (IL)-6 production, and expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), were also reduced by luteolin in a concentration-dependent manner. Furthermore, luteolin suppressed activation of NFκB and its upstream molecular factor, Akt. These results suggest that the protection mechanism of luteolin is by inhibition of NFκB activation possibly via Akt

Isolated tracheal injury after whiplash

AbstractWhiplash, a sudden acceleration–deceleration movement that can cause diverse symptoms such as neck pain, cervicogenic headache, restricted neck movement, tingling of the arms (central cord syndrome), and dizziness. However, laryngotracheal injuries after whiplash are extremely rare. We report the case of a 25-year-old Taiwanese female who presented to the emergency department with severe posterior midline neck pain after a rear-end motorcycle collision. Her C-spine X-ray showed no definite fracture; furthermore, her neck noncontrast-enhanced CT scan revealed paratracheal free air. She was discharged uneventfully after a 12-h observation period. Laryngotracheal injuries after whiplash, a hyperextension–hyperflexion movement, are potentially life-threatening and could lead to airway obstruction. Such injuries should not be overlooked. To the best of our knowledge, this is the first case report of isolated laryngotracheal injury after whiplash

Prognosis of ductal adenocarcinoma of pancreatic head with overexpression of CD44

SummaryBackgroundThe long-term survival rate of patients with pancreatic ductal adenocarcinoma (PDAC) is very low. Cancer stem cells have been identified in PDAC based on the expression of the surface markers CD24, CD44, CD133, and epithelial specific antigen. The prognosis of PDAC may be related to the presence or absence of tumor cells with cancer stem cell surface markers.MethodsEighty-six PDAC patients (51 male and 35 female patients) who underwent surgical treatment at Chang Gung Memorial Hospital—Lin-Kou Medical Center, Lin-Kou, Taiwan between 1998 and 2007 were included in this study. The patients' ages ranged from 30 years to 84 years. All their surgical specimens showed invasive ductal cancer. Immunohistochemical staining with CD44 antibodies was performed. The differences in clinical data, cell types of tumors, tumor staging, and survival rates between patients with CD44− (Group A; n = 33) and CD44+ (Group B; n = 53) were compared.ResultsClinical data, cell types of tumors, and tumor staging between the two groups showed no significant differences. The 3- and 5-year survival rates were, respectively, 51.5% and 19.8% in patients with CD44− tumor cells and 4.0% and 2.0% in those with CD44+ tumor cells. The differences were statistically significant (p < 0.0001). The median overall survival times of the two groups were also different (36.9 months vs. 12.2 months, p < 0.0001). Multivariate analysis showed that the CD44 as well as lymph node status, and differentiation of tumor cells were prognostic factors for patients with PDAC.ConclusionThe results suggested that CD44 expression in patients with PDAC after surgery was significantly associated with decreased survival, whereas patients with CD44− tumor cells survived significantly longer