Feasibility Study on Automatic Interpretation of Radiation Dose Using Deep Learning Technique for Dicentric Chromosome Assay.

The interpretation of radiation dose is an important procedure for both radiological operators and persons who are exposed to background or artificial radiations. Dicentric chromosome assay (DCA) is one of the representative methods of dose estimation that discriminates the aberration in chromosomes modified by radiation. Despite the DCA-based automated radiation dose estimation methods proposed in previous studies, there are still limitations to the accuracy of dose estimation. In this study, a DCA-based automated dose estimation system using deep learning methods is proposed. The system is comprised of three stages. In the first stage, a classifier based on a deep learning technique is used for filtering the chromosome images that are not appropriate for use in distinguishing the chromosome; 99% filtering accuracy was achieved with 2,040 test images. In the second stage, the dicentric rate is evaluated by counting and identifying chromosomes based on the Feature Pyramid Network, which is one of the object detection algorithms based on deep learning architecture. The accuracies of the neural networks for counting and identifying chromosomes were estimated at over 97% and 90%, respectively. In the third stage, dose estimation is conducted using the dicentric rate and the dose-response curve. The accuracies of the system were estimated using two independent samples; absorbed doses ranging from 1- 4 Gy agreed well within a 99% confidential interval showing highest accuracy compared to those in previous studies. The goal of this study was to provide insights towards achieving complete automation of the radiation dose estimation, especially in the event of a large-scale radiation exposure incident.

Aggravation of Relapsing Polychondritis due to the Infection and Its Manifestation on a Nasal Tip Graft.

Relapsing polychondritis (RP) is an uncommon systemic disease that is characterized by episodic and progressive inflammation of the cartilaginous structures, which can be very debilitating and in some instances life-threatening. The pathogenic pathways of RP are largely unknown. However, several hypothesis have been suggested. We had an interesting case of aggravation of RP due to the infection. Graft cartilage on the nasal tip was affected by RP also. This case can give a clue of revealing the pathogenesis of RP. We introduce a case with a review of the literature.

The expression of adiponectin receptor is altered in mild and moderate/severe persistent allergic nasal mucosa.

BACKGROUND: Adiponectin, one of the adipokines, has been implicated in the inflammatory process in patients with allergic rhinitis. The level of adiponectin is affected by immunotherapy. Considering the fact that adiponectin receptors (AdipoRs) mediate intracellular signaling events in response to the binding of adiponectin, the role of AdipoRs in healthy and allergic nasal mucosa should be determined. This study investigates the level of expression and distribution pattern of AdipoR1 and AdipoR2 in healthy, mild, and moderate/severe persistent allergic nasal mucosa to understand the role of adiponectin in allergic rhinitis. METHODS: The level of expression and distribution pattern of AdipoR1 and AdipoR2 were evaluated in healthy, mild, and moderate/severe persistent allergic nasal mucosa, using semiquantitative reverse-transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot analysis. RESULTS: AdipoR1 was expressed in healthy, mild, and moderate/severe persistent allergic nasal mucosa where it was commonly localized to the vascular endothelium. However, AdipoR2 was not expressed in any samples of nasal mucosa tested in the present study. Semiquantitative RT-PCR and Western blot analysis showed that the level of expression of AdipoR1 mRNA and protein was decreased in mild and moderate/severe persistent allergic nasal mucosa in comparison with healthy nasal mucosa, but not significantly different between mild and moderate/severe persistent allergic nasal mucosa. CONCLUSION: These results indicate that AdipoR1 may play an important role in the pathogenesis of allergic nasal mucosa, suggesting a role for AdipoR1 in vascular dysfunction in mild and moderate/severe persistent allergic nasal mucosa.

Efficacy of single-staged modified uvulopalatopharyngoplasty with nasal surgery in adults with obstructive sleep apnea syndrome.

OBJECTIVE: The aim of this study was to investigate the clinical efficacy of single-staged modified uvulopalatopharyngoplasty (UPPP) with nasal surgery and the relationship between its surgical outcomes and an anatomy-based staging system in patients with obstructive sleep apnea syndrome (OSAS) with nasal obstruction. STUDY DESIGN AND SETTING: Before-after analysis at a university hospital. SUBJECTS AND METHODS: A total of 41 consecutive OSAS patients (mean age 40.1 ± 7.3 years) who underwent single-staged modified (uvula-preserving) UPPP with nasal surgery were included. The investigators compared subjective symptoms and polysomnographic data before and after surgery and investigated objective surgical outcomes according to the anatomy-based (Friedman) staging system and postoperative complications. Surgical success was defined as a reduction of at least 50% in preoperative apnea-hypopnea index (AHI) and a postoperative AHI of less than 20 per hour. RESULTS: After simultaneous nasal-oropharyngeal surgery, the AHI significantly decreased (from 45.9 ± 23.4 to 20.9 ± 22.1 events per hour; P < .001) and the overall success rate was 56.1% (23/41). Surgical success rates in stages I, II, and III were 70.6% (12/17), 60.0% (9/15), and 22.2% (2/9), respectively. There were no major complications during or after surgery, and most minor complications were transient and resolved without morbidity. CONCLUSIONS: Single-staged modified UPPP with nasal surgery is an available and relatively safe surgical approach in OSAS patients with nasal obstruction. To achieve the best possible surgical outcomes, it is important to select appropriate patients using the anatomy-based staging system.

Increased expression of arginase I and II in allergic nasal mucosa.

OBJECTIVES/HYPOTHESIS: It is known that arginase may be a regulator of diverse pathways, including production of nitric oxide (NO). Increased expression of arginase has been reported in several inflammatory lung diseases, including allergic asthma, suggesting that this may be a common feature underlying the pathophysiology of airway hyperreactivity. Thus, arginase I and II may play a role in the pathogenesis of allergic rhinitis. The distribution pattern and level of expression of arginase I and II were therefore determined in normal and allergic nasal mucosa. STUDY DESIGN: Controlled, prospective study. METHODS: The distribution pattern and level of expression of arginase I and II in normal and allergic nasal mucosa were evaluated using RT-PCR, immunohistochemistry, and Western blotting. RESULTS: The level of expression of arginase I and II mRNA was increased in allergic nasal mucosa in comparison with normal nasal mucosa. In normal nasal mucosa, arginase I and II were expressed in the surface epithelium, submucosal glands, vascular endothelium, and fibroblasts. In allergic nasal mucosa, both enzymes were also localized to similar sites, in addition to inflammatory cells, and the level of expression were greatly increased compared with normal nasal mucosa. These findings were verified by Western blotting. CONCLUSIONS: These results indicate that arginase I and II may play a role in the pathophysiology of allergic rhinitis, and suggest the possible role of the L-arginine metabolic pathway through modulation of L-arginine availability as a substrate for nitric oxide synthase (NOS) and arginase in the pathogenesis of allergic rhinitis.

Increased expression of acidic mammalian chitinase and chitotriosidase in the nasal mucosa of patients with allergic rhinitis.

OBJECTIVES/HYPOTHESIS: Acidic mammalian chitinase (AMCase) has emerged as an important mediator of allergic asthma in both animal models and in humans. Recently, chitotriosidase has been suggested to play a role in innate immunity because of its phagocytic-specific expression. Thus, AMCase and chitotriosidase may play a role in the pathogenesis of allergic nasal mucosa. The expression and pattern of distribution of AMCase and chitotriosidase were, therefore, determined in normal and allergic nasal mucosa. STUDY DESIGN: Controlled, prospective study. METHODS: Normal inferior turbinate mucosa was obtained in patients who were admitted for augmentation rhinoplasty. Allergic turbinate mucosa was obtained from patients who had perennial allergic rhinitis during septo-turbinate surgery. Reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blotting were applied to the normal and allergic nasal mucosa. RESULTS: The expression of AMCase and chitotriosidase mRNAs and proteins analyzed by RT-PCR and Western blot were detected in all normal and allergic turbinate mucosa tested. The levels of expression of AMCase and chitotriosidase mRNAs and proteins were increased in allergic turbinate mucosa compared with normal turbinate mucosa. In both normal and allergic turbinate mucosa, AMCase and chitotriosidase were detected in the epithelium, inflammatory cells, and submucosal glands. The staining intensity for AMCase and chitotriosidase was stronger in allergic nasal mucosa than normal nasal mucosa. CONCLUSIONS: AMCase and chitotriosidase are constitutively expressed in normal turbinate mucosa, suggesting involvement in defense against chitin-containing pathogens. Upregulation of these chitinases in allergic condition suggests that they may play a role in the nasal allergic reaction like other inflammatory mediators in allergic rhinitis. Laryngoscope, 2010.

Role of NADPH oxidase-2 in lipopolysaccharide-induced matrix metalloproteinase expression and cell migration.

This study examined the hypothesis that the control of NADPH oxidase-2 (Nox2)-mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Lipopolysaccharide (LPS) stimulation of Raw264.7 cells and mice peritoneal macrophages increased the expression of MMP-9, 10, 12 and 13 mRNA, and also increased Raw264.7 cell migration. Treatment with an antioxidant (N-acetyl cysteine) or Nox inhibitors strongly inhibited the expression of MMPs by LPS and inhibited cell migration. LPS caused ROS production in macrophages and increased the mRNA expression of Nox isoforms Nox1 and Nox2 by 20-fold and two-fold, respectively. While Nox1 small interfering RNA (siRNA) did not inhibit LPS-mediated expression of MMPs, Nox2 siRNA inhibited the expressions of MMP-9, 10 and 12. Neither Nox1 nor Nox2 siRNA influenced the LPS-mediated expression of MMP-13. In addition, NAC or apocynin attenuated LPS-induced ROS production and MMP-9 expression. MMP-9 expression and cell migration were controlled by ERK1/2-ROS signaling. Collectively, these results suggest that LPS stimulates ROS production via ERK and induce various types of MMPs expression and cell migration.

Increased expression of glycoprotein 340 in the ethmoid sinus mucosa of patients with chronic sinusitis.

OBJECTIVES: To investigate the expression and distribution of glycoprotein 340 (gp340), a secretory glycoprotein, in normal human sinus mucosa and inflammatory sinus mucosa and evaluate the possible effects of gp340 on the development of chronic sinusitis. Glycoprotein 340 was identified as a key element in the innate host defense mechanism on many mucosal surfaces and is directly involved in defense functions aimed at clearing gram-positive and gram-negative bacteria. DESIGN: Prospective study. SETTING: Tertiary academic institution. PATIENTS: Normal sinus mucosa was obtained from the ethmoid sinus mucosa of 8 patients with blowout fractures undergoing endoscopic reduction. Inflammatory sinus mucosa was taken from 25 patients with chronic polypoid sinusitis during endoscopic sinus surgery. INTERVENTION: Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemical analysis, and Western blotting were performed. MAIN OUTCOME MEASURES: The expression level and distributional pattern of gp340 in normal and inflammatory sinus mucosa were analyzed. RESULTS: Transcripts of the gp340 gene were detected in all human sinus tissues analyzed by RT-PCR. Immunohistochemical analysis revealed that gp340 is mainly localized in submucosal gland of both normal and inflammatory sinus mucosa. Semiquantitative RT-PCR and Western blot analysis showed the increased expression levels of gp340 in the inflammatory sinus mucosa compared with the normal sinus mucosa. CONCLUSION: These results suggest that gp340 may play a constitutive role in nasal defense and may be up-regulated in response to inflammation, participating in antimicrobial defense in chronic sinusitis.

Differential gene expression profiles in salicylate ototoxicity of the mouse.

CONCLUSION: This study demonstrated differential gene expression profiles in salicylate ototoxicity with oligonucleotide microarray. This study may also provide basic information on candidate genes associated with hearing loss and/or tinnitus or recovery after salicylate-induced cochlear dysfunction. OBJECTIVES: Salicylate ototoxicity is accompanied by temporary hearing loss and tinnitus. The purpose of the present study was to evaluate the gene expression profiles in the mouse cochlea with salicylate ototoxicity using DNA microarray. MATERIALS AND METHODS: The subject mice were injected intraperitoneally with 400 mg/kg of sodium salicylate; an approximate 30 dB threshold shift that was observed by auditory brainstem response was achieved 3 h after an injection of sodium salicylate and the hearing threshold returned to within normal range at 3 days. Differential gene expression profiles at 3 h after salicylate injection in comparison to the normal cochlea were analyzed with DNA microarray technology. RESULTS: No ultrastructural changes in the mice cochlea were observed by TEM at 3 h after salicylate injection. Microarray revealed that 87 genes were up-regulated twofold or more in the mouse cochlea with salicylate ototoxicity in comparison to the normal cochlea. Among these genes, increased expression levels of 30 functional genes were confirmed by semi-quantitative RT-PCR.

D2-40 immunohistochemical assessment of lymphangiogenesis in normal and edematous sinus mucosa and nasal polyp.

OBJECTIVE: The lymphatic system plays an important role in the maintenance of tissue fluid homeostasis, which facilitates interstitial protein transport. Until recently, the lymphatic system of the sinonasal mucosa has been relatively poorly studied. The authors aimed to investigate the distributional and quantitative changes of the lymphatic vessels in inflammatory sinus mucosa and nasal polyps in comparison with healthy sinus mucosa using D2-40 antibody. METHODS: Immunohistochemistry and Western blotting with D2-40 antibody were applied to normal and edematous ethmoid sinus mucosa and nasal polyps. The number, size, and length densities of lymphatic vessels were evaluated using tissue sections and whole mount preparations. RESULTS: Most lymphatic vessels in normal and edematous ethmoid sinus mucosa were distributed in the subepithelial layer. Some of these vessels were dilated, whereas others were compressed and had a slit-like lumen. No D2-40 positive vessels were found in samples of nasal polyps. Lymphatic vessels showed no statistically significant difference in their number, size, or length density between normal and edematous ethmoid sinus mucosa. Western blot also showed no differences in their expression levels. CONCLUSION: These findings indicate that lymphangiogenesis does not occur in edematous ethmoid sinus mucosa, which may not reuptake interstitial fluid efficiently in inflammatory conditions, resulting in the formation of mucosal edema in chronic inflammation.