Nasal bone fractures are the most common type of facial fractures. Previous studies have shown that most nasal fractures involve the septum, which can provide an obstacle to the successful reduction of nasal bone fractures. In particular, septal fractures in combination with simple nasal bone fractures are usually unrecognized and untreated at the time of injury. Furthermore, systemized treatment protocols and diagnostic tools for septal fractures in the case of simple nasal bone fracture have not previously been presented. In this study, the clinical findings of septal fractures in cases of simple nasal bone fracture were correlated with symptoms, signs, and computed tomography findings and assessed statistically. The patterns of septal fractures in simple nasal bone fractures were assessed by direct vision via hemitransfixion incision. Of the 52 patients with simple nasal bone fracture who presented over a 3-year period and were included in this study, 10 were female and 42 were male, with an average age of 33.8 years (age range, 18 to 61 years). Fifty of these patients (96.2 percent) showed septal fractures, and septoplasty or submucosal resection was performed on 41 patients (78.8 percent) who manifested severe septal fractures of perioperative septal grade 3 or higher. Closed reduction of the nasal bone fracture only was performed on the remaining 11 patients. Among the signs evident at physical examination, mucosal tearing was found to be statistically significant for septal fracture. Computed tomography was found to be very helpful in diagnosing septal fracture but could not predict its severity accurately (Spearman correlation coefficient between computed tomography septal grading and perioperative septal grading, 33.5 percent). Therefore, computed tomography could not be used as a definitive diagnostic modality for septal fractures in terms of deciding whether septoplasty or submucous resection was needed. It is evident that septal fractures are frequent in simple nasal bone fractures that are not combined with other facial bone fractures. This study confirms that there are differences between radiologic findings and perioperative findings. To reduce the incidence of posttraumatic nasal deformity, meticulous physical examinations with subsequent septoplasty or submucosal resection are needed in the treatment of simple nasal bone fracture.

Both oxidative stress and endoplasmic reticulum (ER) stress are known to contribute to secondary injury, ultimately leading to cell death after spinal cord injury (SCI). Here, we showed that valproic acid (VPA) reduced cell death of motor neurons by inhibiting cytochrome c release mediated by oxidative stress and ER stress after SCI. After SCI, rats were immediately injected with VPA (300 mg/kg) subcutaneously and further injected every 12 h for an indicated time period. Motor neuron cell death at an early time after SCI was significantly attenuated by VPA treatment. Superoxide anion (O2-) production and inducible NO synthase (iNOS) expression linked to oxidative stress was increased after injury, which was inhibited by VPA. In addition, VPA inhibited c-Jun N-terminal kinase (JNK) activation, which was activated and peaked at an early time after SCI. Furthermore, JNK activation and c-Jun phosphorylation were inhibited by a broad-spectrum reactive oxygen species (ROS) scavenger, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), indicating that ROS including O2- increased after SCI probably contribute to JNK activation. VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor. The levels of phosphorylated Bim and Mcl-1, which are known as downstream targets of JNK, were significantly reduced by SP600125. On the other hand, VPA treatment inhibited ER stress-induced caspase-12 activation, which is activated in motor neurons after SCI. In addition, VPA increased the Bcl-2/Bax ratio and inhibited CHOP expression. Taken together, our results suggest that cell death of motor neurons after SCI is mediated through oxidative stress and ER stress-mediated cytochrome c release and VPA-inhibited cytochrome c release by attenuating ROS-induced JNK activation followed by Mcl-1 and Bim phosphorylation and ER stress-coupled CHOP expression.

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