Object The current study evaluates the incidence of anatomical variations of the V3 segment of the vertebral artery (VA) and the posterior arch of the atlas (C-1). Failure to appreciate these types of anatomical variations can cause catastrophic injury to the VA during posterior approaches to the upper cervical spine. Methods In the present study, the authors analyzed the records of 1013 Korean patients who underwent computed tomography (CT) angiography to evaluate the incidence of anomalous variations in the third segment of the VA and to determine the incidence and morphometric characteristics of any detected posterior ponticuli. The authors also hoped to determine any specific imaging features that might indicate a VA anomaly around the craniovertebral junction. Results The mean age of the patients was ~ 55.7 years and the prevalence of a posterior ponticulus was 15.6%. The incidence rate of a posterior ponticulus in the male population was 19.3%, whereas in the female population it was 12.8%. The incomplete type of posterior ponticulus was more common than the complete type. The mean age of the patients with an incomplete posterior ponticulus (55.7 years) was significantly younger (p = 0.018) than the mean age of patients with a complete posterior ponticulus (57.6 years). The incidence rate of a persistent first inter-segmental artery was 4.7% and the incidence rate of a fenestrated VA was 0.6%. The area of the C-1 transverse foramen on the abnormal side was significantly smaller than that of the contralateral normal side. Conclusions The shape of the C-1 posterior arch and the third segment of the VA are heterogeneous. Therefore, preoperative radiological studies should be performed to identify any anatomical variations. Using preoperative 3D CT angiography, we can precisely identify an anomalous VA and significantly reduce the risk of VA injury.

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✓ Atlantoaxial fixation in which C1–2 screw–rod fixation is performed is a relatively new method. Because reports about this technique are rather scant, little is known about its associated complications. In this report the authors introduce hypoglossal nerve palsy as a complication of this novel posterior atlantoaxial stabilization method. A 67-year-old man underwent a C1–2 screw–rod fixation for persistent neck pain resulting from a Type 2 odontoid fracture that involved disruption of the transverse atlantal ligament. Posterior instrumentation in which a C-1 lateral mass screw and C-2 pedicle screw were placed was performed. Postoperatively, the patient suffered dysphagia with deviation of the tongue to the left side. At the 4-month follow-up examination, bone fusion was noted on plain x-ray studies of the cervical spine. His hypoglossal nerve palsy resolved completely 2 months postoperatively. To the authors’ knowledge, this is the first report in the literature of hypoglossal nerve palsy following C1–2 screw–rod fixation. The hypoglossal nerve is one of the structures that can be damaged during C-1 lateral mass screw placement.

Brachial plexus injury (BPI) is a severe peripheral nerve injury affecting upper extremities, causing functional damage and physical disability. The most common cause of adult BPI is a traffic accident, and the incidence has steadily increased since the 1980s. BPIs can be divided into three types; preganglionic lesion, postganglionic lesion, and a combination of both. Whether the continuation of the root and the spinal cord is preserved is a critical factor in determining the treatment strategy. The level of lesion can be analogized by clinical manifestations. But imaging studies including computed tomography (CT) myelography and magnetic resonance imaging (MRI) as well as electrodiagnostic studies are helpful in diagnosis of BPI. If diagnostic electromyography suggests that the damage is non-degenerative, conservative management is indicated. However, a reconstructive plan should be formulated, when there is no evidence of spontaneous recovery within 6 months of injury. Operative options used in BPI include nerve grafting, neurotization (nerve transfer), and other brachial plexus reconstructive techniques including the transplantation of various structures. In this review article, the mechanism and classification of injury, clinical manifestations, updated diagnostic studies, recent treatment strategies, and pain after BPI would be discussed.

Expression of BMP-4 of epithelial cells was higher in OLP than NOM. High concentration of BMP-4 caused an apoptosis of oral epithelial cells in oral mucosa organ culture. Therefore, over-expression of BMP-4 is one causing factor for apoptosis of oral epithelial cells through upregulation of p53, MMP1 and MMP3 in OLP.

Insulin resistance plays an important role in the development of type 2 diabetes mellitus. Scopoletin, a phenolic coumarin, is reported to regulate hyperglycemia and diabetes. To examine its effect on insulin resistance, we treated high-glucose-induced, insulin-resistant HepG2 cells with scopoletin and measured phosphatidylinositol 3-kinase (PI3 K)-linked protein kinase B (Akt/PKB) phosphorylation. Scopoletin significantly stimulated the reactivation of insulin-mediated Akt/PKB phosphorylation. This effect was blocked by LY294002, a specific PI3 K inhibitor. The ability of scopoletin to activate insulin-mediated Akt/PKB was greater than that of rosiglitazone, a thiazolidinedione, and scopoletin was less adipogenic than rosiglitazone, as shown by the extent of lipid accumulation in differentiated adipocytes. Scopoletin increased the gene expression of both peroxisome proliferator-activated receptor γ2 (PPARγ2), a target receptor for rosiglitazone, and adipocyte-specific fatty acid binding protein, but not to the level induced by rosiglitazone. However, the PPARγ2 protein level was increased equally by rosiglitazone and scopoletin in differentiated adipocytes. Our results suggest that scopoletin can ameliorate insulin resistance in part by upregulating PPARγ2 expression. With its lower adipogenic property, scopoletin may be a useful candidate for managing metabolic disorders, including type 2 diabetes mellitus.

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It remains unclear whether patients with non-small-cell lung cancer (NSCLC) develop brain metastasis during or after standard therapy. We attempted to identify biological markers that predict brain metastasis, and investigated how to modulate expression of such markers. A case-control study of patients who were newly diagnosed with NSCLC and who had developed brain metastasis during follow-up was conducted between 2004 and 2009. These patients were compared with a control group of patients who had NSCLC but no evidence of brain metastasis. Immunohistochemical analysis of expression of Ki-67, p53, Bcl-2, Bax, vascular endothelial growth factor, epidermal growth factor receptor, caspase-3, and E-cadherin was conducted. The methylation status of the genes for O(6)-methylguanine-DNA-methyltransferase, tissue inhibitor of matrix metalloproteinase (TIMP)-2, TIMP-3, and death-associated protein-kinase was also determined, by use of a methylation-specific polymerase chain reaction. A significantly increased risk of developing brain metastasis was associated with the presence of primary tumors with low E-cadherin expression in patients with NSCLC. We also investigated the effects of pioglitazone, a peroxisome proliferator-activated receptor γ-activating drug, in tumor-bearing mouse models. We found that E-cadherin expression was proportional to pioglitazone exposure time. Interestingly, pioglitazone pretreatment before cancer cell inoculation prevented loss of E-cadherin expression and reduced expression of MMP9 and fibronectin, compared with the control group. E-cadherin expression could be a predictor of brain metastasis in patients with NSCLC. Preventive treatment with pioglitazone may be useful for modulating E-cadherin expression.