A Case of Traumatic Nasal Valve Stenosis Successfully Treated with Open Rhinoplasty and Z-Plasty.

External nasal deformity is common and can be treated surgically. It often occurs in conjunction with the development of the nasal septal cartilage, vomer, and vertical plate of the ethmoid bone but may be caused by trauma. Here, we present a case of external nasal deformity caused by trauma. A woman presented with nasal obstruction due to dysfunction of the nasal valve area and was referred to our department for treatment. No chronic rhinosinusitis or nasal septal deviation that causes nasal obstruction was noted at the initial examination. However, trauma-related scarring was observed in the nasal valve area, and a Cottle test yielded positive results. The patient underwent combined rhino- and Z-plasty surgery and is currently undergoing follow-up at an outpatient clinic.Although otolaryngologists generally use an endonasal approach to treat nasal obstruction, it is important to perform an appropriate evaluation of the external nose and to collaborate with a plastic surgeon, as necessary.

Osteitis in Eosinophilic Chronic Rhinosinusitis.

OBJECTIVES: Eosinophilic chronic rhinosinusitis (ECRS) is an allergic inflammatory disease characterized by chronic inflammation of the sinus mucosa, and sometimes, osteitis. This study aimed to investigate the pattern of osteitis in ECRS and the relationship between bony thickening of the middle turbinate and recurrence of ECRS. METHODS: A total of 246 patients with paranasal diseases were included in the study. The patients' data on bone thickening level, mucosal thickening, polyp score, clinical severity, and laboratory data were retrospectively evaluated. RESULTS: In total, 38, 186, and 22 patients had ECRS, non-ECRS (NECRS), and odontogenic sinusitis, respectively. The Lund-Mackey (LM) score and Global Osteitis Scoring Scale (GOSS) scores in patients with ECRS were higher than those in patients with other paranasal diseases. There was a significant positive correlation between the GOSS score and ECRS clinical disease severity. Postoperative recurrence was significantly increased in patients with ECRS associated with bony thickening of the middle turbinate. CONCLUSION: Both mucosal inflammation and osteitis were more severe in patients with ECRS than in patients with other diseases, and clinical disease severity was correlated with osteitis. Furthermore, the postoperative recurrence rate tended to increase in patients with ECRS who had bony thickening of the middle turbinate.

Osteitis in Diseases With Unilateral Opacification of Paranasal Sinuses.

OBJECTIVES: Chronic rhinosinusitis (CRS) is a common disease with mucosal inflammation, and may sometimes be accompanied by bone thickening. The disease is usually bilateral; when it is unilateral, there may be a specific disease. This study aimed to investigate the association between unilateral sinus opacification and osteitis. METHODS: In total, 104 patients with computed tomography revealing unilateral sinus opacification were included in this study. Patients were retrospectively evaluated using the Global Osteitis Scoring Scale (GOSS) score, Lund-Mackey (LM) score, polyp score, and blood tests. RESULTS: In total, 47, 11, 9, 17, and 20 patients had CRS, paranasal sinus cyst, inverted papilloma, mycetoma, and odontogenic sinusitis, respectively. The GOSS score in patients with mycetoma was higher than that in patients with CRS. However, no significant differences in the GOSS scores between patients with mycetoma, inverted papilloma, and odontogenic sinusitis existed. 10 of the 104 patients had osteitis with extensive bone thickening and a GOSS score of 4 or higher. Patients with CRS and mycetoma tended to have a higher GOSS score for the maxillary sinus than for the other sinuses. There was a significant positive correlation between the GOSS score and LM score in patients with diseases other than paranasal sinus cyst. CONCLUSIONS: Mycetoma is more likely to cause osteitis than CRS, and a unique mechanism of osteitis exacerbation is predicted. As there is a positive correlation between bone thickening and sinus inflammation, a close association between osteitis and mucosal inflammation is inferred in diseases involving unilateral sinus opacification.

Localization of KRAS downstream target ARL4C to invasive pseudopods accelerates pancreatic cancer cell invasion.

Pancreatic cancer has a high mortality rate due to metastasis. Whereas KRAS is mutated in most pancreatic cancer patients, controlling KRAS or its downstream effectors has not been succeeded clinically. ARL4C is a small G protein whose expression is induced by the Wnt and EGF-RAS pathways. In the present study, we found that ARL4C is frequently overexpressed in pancreatic cancer patients and showed that its localization to invasive pseudopods is required for cancer cell invasion. IQGAP1 was identified as a novel interacting protein for ARL4C. ARL4C recruited IQGAP1 and its downstream effector, MMP14, to invasive pseudopods. Specific localization of ARL4C, IQGAP1, and MMP14 was the active site of invasion, which induced degradation of the extracellular matrix. Moreover, subcutaneously injected antisense oligonucleotide against ARL4C into tumor-bearing mice suppressed metastasis of pancreatic cancer. These results suggest that ARL4C-IQGAP1-MMP14 signaling is activated at invasive pseudopods of pancreatic cancer cells.

Most cases of pancreatic cancer are detected in the later stages when they are difficult to treat and, as a result, survival is low. Over 90% of pancreatic cancers contain genetic changes that increase the activity of a protein called KRAS. This hyperactive KRAS drives cancer growth and progression. Attempts to treat pancreatic cancer using drugs that reduce the activity of KRAS have so far failed. The KRAS protein can accelerate growth in healthy cells as well as in cancer and it does this by activating various other proteins. Drugs that target some of these other proteins could be more effective at treating pancreatic cancer than the drugs that target KRAS. One of these potential targets is called ARL4C. ARL4C is active during fetal development, but it is often not present in adult tissues. Harada et al. investigated whether the protein is important in pancreatic cancer, and what other roles it has in the body, to better understand if it is a good target for cancer treatment. First, Harada et al. used cells grown in the lab to show that ARL4C contributes to the aggressive spread of human pancreatic cancers. Using mice, Harada et al. also showed that blocking the activity of ARL4C in pancreatic cancers helped to slow their progression. Harada et al.'s results suggest that ARL4C could be a good target for new drugs treating pancreatic cancers. Given that this protein does not seem to have important roles in the cells of adults, targeting it is unlikely to have major side effects. Further investigation of ARL4C in more human-like animal models will help to confirm these results.