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CpG oligodeoxunucleotide (ODN) plays an important role in immune cell function. The present study examined whether temporal control of toll-like receptor (TLR)-9 by CpG ODN can regulate the expression of matrix metalloproteinase-9 (MMP-9). CpG ODN induced the release of tumor necrosis factor (TNF)-alpha and the expression of TNF receptor (TNFR)-II, but not of TNFR-I, in a time-dependent manner and stimulated significant, though delayed, MMP-9 expression. The endosomal acidification inhibitors, chloroquine or bafilomycin A, inhibited CpG ODN-induced TNF-alpha, TNFR-II, and MMP-9 expression. CpG ODN induced the phosphorylation of Akt, and the inhibition of Akt by LY294002 suppressed CpG ODN-induced TNF-alpha, TNFR-II, and MMP-9 expressions. Moreover, neutralizing TNF-alpha antibody significantly suppressed CpG ODN-induced MMP-9 expression, suggesting the involvement of TNF-alpha. These observations suggest that CpG ODN may play important roles in macrophage activation by regulating the expression of MMP-9 via a TLR-9/Akt/TNF-alpha-dependent signaling pathway.

The present study investigated the role of peripheral group I and II metabotropic glutamate receptors (mGluRs) in interleukin-1beta (IL-1beta)-induced mechanical allodynia in the orofacial area. Experiments were carried out on Sprague-Dawley rats weighing between 230 and 280 g. After subcutaneous administration of 0.01, 0.1, 1, or 10 pg of IL-1beta, we examined withdrawal behavioral responses produced by 10 successive trials of a ramp of air-puffs pressure applied ipsilaterally or contralaterally to the IL-1beta injection site. The thresholds of air puffs were measured 10, 30, 60, 120, or 180 min after 25 microl of IL-1beta was administered through an implanted tube. Subcutaneous injection of IL-1beta produced bilateral mechanical allodynia. While the IL-1beta-induced mechanical allodynia was blocked by pretreatment with an IL-1 receptor antagonist, the IL-1beta-induced mirror-image mechanical allodynia was not blocked by an IL-1 receptor antagonist injected into the contralateral side. Subcutaneous administration of CPCCOEt or LY367385, an mGluR1 antagonist, or MPEP or SIB1893, an mGluR5 antagonist, 10 min prior to injection of IL-1beta abolished IL-1beta-induced mechanical allodynia. Pretreatment with APDC or DCG4, a group II mGluR agonist, blocked the IL-1beta-induced mechanical allodynia. The anti-allodynic effect induced by APDC was inhibited by pretreatment with LY341495, a group II mGluR antagonist. These results suggest that peripheral group I and II mGluRs participate in IL-1beta-induced mechanical allodynia in the orofacial area. Peripheral group I mGluR antagonists blocked the IL-1beta-induced mechanical allodynia, while peripheral group II mGluR agonists produced anti-allodynic effects on IL-1beta-induced mechanical allodynia in the orofacial area of rats.

The present study investigated the effects of intracisternal administration of MCP-1, Rantes or IL-8 on pain transmission in the orofacial area. We also investigated mechanisms of hyperalgesic responses produced by intracisternal administration of IL-8. An orofacial formalin test was employed to assess the effects of chemokines on nociceptive processing. For each animal, the number of behavioral responses and the time spent grooming, rubbing and/or scratching the facial region proximal to the formalin injection site was recorded for nine successive 5-min intervals. Intracisternal administration of MCP-1, Rantes or IL-8 significantly increased formalin-induced scratching behavioral responses in the orofacial area. Intracisternal pretreatment with indomethacin, a non-selective cyclooxygenase inhibitor, did not block IL-8-induced hyperalgesia. Pretreatment with 100 microg propranolol, a non-selective beta-adrenergic receptor antagonist and 50 microg atenolol, a selective beta(1)-adrenergic receptor antagonist, inhibited the number of scratches and the duration of scratching produced by 1 ng of IL-8 injected intracisternally. These results indicate that intracisternal administration of chemokines produce a hyperalgesic response with an orofacial inflammatory pain model and that the IL-8-induced hyperalgesia is mediated by central beta(1)-adrenergic receptor.

Given its contribution to malignant phenotypes of cancer, tumor hypoxia has been considered as a potential therapeutic problem. In the stressful microenvironment condition, hypoxia inducible factor 1 (HIF1) is well known to mediate the transcriptional adaptation of cells to hypoxia and acts as a central player for the process of hypoxia-driven malignant cancer progression. Here, we found that irradiation causes the HIF1α protein to stabilize, even in normoxia condition through activation of p38 MAPK, thereby promoting angiogenesis in tumor microenvironment and infiltrative property of glioma cells. Notably, irradiation reduced hydroxylation of HIF1α through destabilization of prolyl hydroxylases (PHD)-2. Moreover, radiation also decreased the half-life of protein von Hippel-Lindau (pVHL), which is a specific E3 ligase for HIF1α. Of note, inhibition of p38 MAPK attenuated radiation-induced stabilization of HIF1α through destabilization of PHD-2 and pVHL. In agreement with these results, targeting of either p38 MAPK, HIF1α, pVHL or PHD-2 effectively mitigated the radiation-induced tube formation of human brain-derived micro-vessel endothelial cells (HB-MEC) and infiltration of glioma cells. Taken together, our findings suggest that targeting HIF1α in combination with ionizing radiation might increase the efficacy of radiotherapy for glioma treatment.

Intraosseous hemangiomas account for 1% of all bone tumors and primarily originate from the vertebral column and skull bones. However, intraosseous hemangiomas of the nasal cavity are extremely rare. Here, we report a case of intraosseous hemangioma with a cavernous pattern arising from the middle turbinate that was preoperatively misdiagnosed as chronic rhinosinusitis with polyps. Except for nasal obstruction, there were no specific rhinologic symptoms. The tumor was excised en bloc by the endoscopic endonasal approach without preoperative embolization.

Reactive oxygen species (ROS) are well known to be involved in oncogene-mediated cellular transformation. However, the regulatory mechanisms underlying ROS generation in oncogene-transformed cells are unclear. In the present study, we found that oncogenic K-Ras induces ROS generation through activation of NADPH oxidase 1 (NOX1), which is a critical regulator for the K-Ras-induced cellular transformation. NOX1 was activated by K-Ras-dependent translocation of p47(phox), a subunit of NOX1 to plasma membrane. Of note, PKCδ, when it was activated by PDPK1, directly bound to the SH3-N domain of p47(phox) and catalyzed the phosphorylation on Ser348 and Ser473 residues of p47(phox) C-terminal in a K-Ras-dependent manner, finally leading to its membrane translocation. Notably, oncogenic K-Ras activated all MAPKs (JNK, ERK and p38); however, only p38 was involved in p47(phox)-NOX1-dependent ROS generation and consequent transformation. Importantly, K-Ras-induced activation of p38 led to an activation of PDPK1, which then signals through PKCδ, p47(phox) and NOX1. In agreement with the mechanism, inhibition of p38, PDPK1, PKCδ, p47(phox) or NOX1 effectively blocked K-Ras-induced ROS generation, anchorage-independent colony formation and tumor formation. Taken together, our findings demonstrated that oncogenic K-Ras activates the signaling cascade p38/PDPK1/PKCδ/p47(phox)/NOX1 for ROS generation and consequent malignant cellular transformation.

Claudins (CLDNs) are a family of integral membrane proteins central to the formation of tight junctions, structures that are involved in paracellular transport and cellular growth and differentiation, and are critical for the maintenance of cellular polarity. Recent studies have provided evidence that CLDNs are aberrantly expressed in diverse types of human cancers, including hepatocellular carcinomas (HCCs). However, little is known about how CLDN expression is involved in cancer progression. In this study, we show that CLDN1 has a causal role in the epithelial-mesenchymal transition (EMT) in human liver cells, and that the c-Abl-Ras-Raf-1-ERK1/2 signaling axis is critical for the induction of malignant progression by CLDN1. Overexpression of CLDN1 induced expression of the EMT-regulating transcription factors Slug and Zeb1, and thereby led to repression of E-cadherin, β-catenin expression, enhanced expression of N-cadherin and Vimentin, a loss of cell adhesion, and increased cell motility in normal liver cells and HCC cells. In line with these findings, inhibition of either c-Abl or ERK clearly attenuated CLDN1-induced EMT, as evidenced by a reversal of N-cadherin and E-cadherin expression patterns, and restored normal motility. Collectively, these results indicate that CLDN1 is necessary for the induction of EMT in human liver cells, and that activation of the c-Abl-Ras-Raf-1-ERK1/2 signaling pathway is required for CLDN1-induced acquisition of the malignant phenotype. The present observations suggest that CLDN1 could be exploited as a biomarker for liver cancer metastasis and might provide a pivotal point for therapeutic intervention in HCC.

The prognosis of breast cancer patients is related to the degree of metastasis. However, the mechanisms by which epithelial tumor cells escape from the primary tumor and colonize at a distant site are not entirely understood. Here, we analyzed expression levels of pituitary tumor-transforming gene-1 (PTTG1), a relatively uncharacterized oncoprotein, in patient-derived breast cancer tissues with corresponding normal breast tissues. We found that PTTG1 is highly expressed in breast cancer patients, compared with normal tissues. Also, PTTG1 expression levels were correlated with the degree of malignancy in breast cancer cell lines; the more migratory and invasive cancer cell lines MDA-MB-231 and BT549 displayed the higher expression levels of PTTG1 than the less migratory and invasive MCF7 and SK-BR3 and normal MCF10A cell lines. By modulating PTTG1 expression levels, we found that PTTG1 enhances the migratory and invasive properties of breast cancer cells by inducing epithelial to mesenchymal transition, as evidenced by altered morphology and epithelial/mesenchymal cell marker expression patterns and up-regulation of the transcription factor Snail. Notably, down-regulation of PTTG1 also suppressed cancer stem cell population in BT549 cells by decreasing self-renewing ability and tumorigenic capacity, accompanying decreasing CD44(high) CD24(low) cells and Sox2 expression. Up-regulation of PTTG1 had the opposite effects, increasing sphere-forming ability and Sox2 expression. Importantly, PTTG1-mediated malignant tumor properties were due, at least in part, to activation of AKT, known to be a key regulator of both EMT and stemness in cancer cells. Collectively, these results suggest that PTTG1 may represent a new therapeutic target for malignant breast cancer.

Synthetic oligodeoxynucleotides (ODNs) with the CpG-motifs are recognized by toll-like receptor 9 (TLR9), which elicits an immune response. Serum starvation of Raw264.7 cells increased tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression. However, treatment with CpG ODN reduced TRAIL expression as well as apoptosis by serum starvation. In serum starved cells, TLR9 inhibitors recovered the decreasing TRAIL expression and sub-G1 accumulation by CpG ODN. CpG ODN-regulated anti-apoptotic signals which were dependent on the Akt-FoxO3a signaling pathway. CpG ODNs activated Akt and inactivated FoxO3a in serum starved cells. Knockdown of FoxO3a by siRNA decreased TRAIL expression and apoptosis in serum-starved cells. In contrast, FoxO3a overexpression increased apoptosis by serum starvation, and CpG ODNs blocked these effects through TRAIL expression. LY294002, a PI3K-Akt inhibitor, blocked the CpG ODN effect of TRAIL expression and the sub-G1 population in serum starved cells. In contrast, overexpression of wild-type Akt reduced additional sub-G1 cells both in non-CpG ODN- and CpG ODN-treated cells. Taken together, these results demonstrate the involvement of Akt-FoxO3a signaling in TLR9-mediated downregulation of TRAIL and anti-apoptotic signals.

Radiation resistance can be overcome by a combination treatment with chemical modifiers. Here, we showed that treatment with 5-bromo-3-(3-hydroxyprop-1-ynyl)-2H-pyran-2-one (BHP), a new 2-pyrone derivative, in combination with ionizing radiation enhances the sensitivity of human cervical cancer cells to ionizing radiation through overproduction of reactive oxygen species (ROS). The combined treatment with BHP and ionizing radiation caused a decrease in clonogenic survival and an increase in apoptotic cell death in cervical cancer cells. The combined treatment promoted conformational activation of Bax and led to mitochondrial apoptotic cell death. The combination treatment also induced a marked increase in intracellular ROS level. Inhibition of ROS attenuated the radiosensitizing effect of BHP, concurrent with a decrease in Bax activation, a decrease in mitochondrial cell death, and an increase in clonogenic survival. These results indicate that BHP synergistically enhances sensitivity of human cervical cancer cells to ionizing radiation through elevation of intracellular ROS and that ROS-dependent Bax activation is critically involved in the increase in apoptotic cell death induced by the combined treatment with BHP and ionizing radiation.

A subpopulation of cancer cells with stem cell properties is responsible for tumor formation, maintenance, and malignant progression; however, the molecular mechanisms underlying the maintenance of cancer stem-like cell properties have remained unclear. Here, we show that the Rho family GTPase Rac1 is involved in the glioma stem-like cell (GSLC) maintenance and tumorigenicity in human glioma. The Rac1-Pak signaling was markedly activated in GSLCs. Knockdown of Rac1 caused reduction of expression of GSLC markers, self-renewal-related proteins and neurosphere formation. Moreover, down-regulation of Rac1 suppressed the migration, invasion, and malignant transformation in GSLCs. Furthermore, inhibition of Rac1 enhanced radiation sensitivity of GSLCs. These results indicate that the small GTPase Rac1 is involved in the maintenance of stemness and malignancies in GSLCs.

The new packaging approach for crystal resonator with quartz crystal is described in this paper. We designed and optimized the structure of wafer level crystal unit package for low cost and high performance with 2.0×1.6×0.45 mm3 size. The crystal unit package is reduced in size and thickness by using a 4" wafer level package technique of general semiconductor process. Traditionally, the package substrate of crystal unit device used ceramics order's HTCC (high temperature co-fired ceramic) and metal lid. The glass and Si wafer for package substrate and lid is chosen and considered as the structure for its mechanical and thermal strength and effective process of mass production. The interconnection via is formed through glass wafer by using sand blasting and Cu electro-plating method that enable the connection of the signal electrode on the quartz blank. The AuSn eutectic bonding between glass package wafer and Si cap wafer that is etched using DRIE (deep reactive ion etch) process protects the quartz blank mechanically and encapsulates high vacuum state. The frequency and impedance performance of wafer level crystal unit in comparison with conventional crystal unit devices is characterized.

The present study is the first demonstration of prolonged nociceptive behavior in the trigeminal region following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats mounted onto a stereotaxic frame under pentobarbital sodium anesthesia. For compression of the trigeminal ganglion, a 4% agar solution (8microl) was injected into the trigeminal ganglion through a stainless steel injector (24 gauge), which extended 2mm beyond the end of a guide cannula (21 gauge). Following agar injection, the injector and guide cannula were removed. In the control group, rats were sham operated without agar injection. Air-puff thresholds (mechanical allodynia), pin prick responses (mechanical hyperalgesia), and spontaneous scratching behavior were examined 3 days before surgery and at 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Data were analyzed using a repeated measures ANOVA followed by multiple group comparisons using the LSD post-hoc test. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and lasted beyond postoperative day 24. Mechanical hyperalgesia was also evident 3 days after compression and persisted until the 40th postoperative day. Although mechanical allodynia and hyperalgesia appeared bilaterally, the ipsilateral side was significantly more sensitive. Intraperitoneal treatment with carbamazepine significantly blocked mechanical allodynia produced by compression of the trigeminal ganglion. These findings suggest that prolonged nociceptive behavior following compression of the trigeminal ganglion may mimic trigeminal neuralgia in this animal model.

Unmethylated CpG oligodeoxynucleotides (CpG ODNs) activate immune cells to produce immune mediators. This study demonstrates that in murine macrophage RAW 264.7 cells, CpG ODN-mediated matrix metalloproteinase-9 (MMP-9) expression is regulated at transcriptional level and requires de novo protein synthesis. Inhibition of ERK and p38 MAPK, but not JNK, results in significant decrease of CpG ODN-induced MMP-9 expression. We found that endosomal maturation inhibitors, chloroquine and bafilomycin A, block CpG ODN-induced ERK and p38 MAPK activation and the subsequent MMP-9 expression. We also observed that CpG ODN induces NF-kappaB activation and NF-kappaB is a downstream target of p38 MAPK. Taken together, our data demonstrate that CpG ODN triggers MMP-9 expression via TLR-9 dependent ERK and p38 MAPK activation followed by NF-kappaB activation.

The present study investigated the role of mitogen-activated protein kinase (MAPK) in orofacial neuropathic pain following chronic constriction injury of the infraorbital nerve (ION-CCI). Experiments were carried out on male Sprague–Dawley rats weighing between 200 and 230 g. The ION was separated from adhering tissue, and two ligatures (5–0 chromic gut) were tied loosely around it. We examined the air-puff thresholds (mechanical allodynia), scores of pinprick (mechanical hyperalgesia), and face grooming frequency for acetone application (hypersensitivity for cold stimulation) − 3, 3, 6, 9, 12, 15, 20, 25, 30, and 40 days after surgery. ION-CCI produced mechanical allodynia, hyperalgesia, and cold hypersensitivity. We investigated whether administration of MAPKs inhibitors blocks ION-CCI-induced mechanical allodynia. Intracisternal administration with PD98059 or SB203580, a MEK inhibitor or a p38 MAPK inhibitor, respectively, significantly inhibited ION-CCI-induced mechanical allodynia in the orofacial area. These results indicate that the ION-CCI produced behavioral alterations in the orofacial area and those central MAPKs pathways contribute to orofacial neuropathic pain. Our findings suggest that MAPKs inhibitors have a potential role in treatment for orofacial neuropathic pain.

The present study investigated the role of peripheral groups I and II metabotropic glutamate receptors (mGluRs) in interleukin (IL)-1beta-induced mechanical allodynia in the orofacial area of rats. Subcutaneous injection of 10 pg of IL-1beta decreased air-puff thresholds ipsilateral or contralateral to the injection site. The decrease in air-puff thresholds appeared 10 min after the injection of IL-1beta and IL-1beta-induced mechanical allodynia persisted for over 3 h. Pre-treatment with 7-(hydroxyimino) cyclopropa[b] chromen-1a-carboxylate ethyl ester (CPCCOEt) or 2-methyl-6-(phenylethynyl)-pyridine hydrochloride (MPEP), a mGluR1 or mGluR5 antagonist, blocked IL-1beta-induced mechanical allodynia and mirror-image mechanical allodynia produced by a subcutaneous injection of 10 pg of IL-1beta. However, post-treatment with CPCCOEt or MPEP did not affect changes in behavioral responses, which were produced by the IL-1beta injection. Pre-treatment, as well as post-treatment with (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC), a group II mGluR agonist, blocked either IL-1beta-induced mechanical allodynia or mirror-image mechanical allodynia. The anti-allodynic effects of APDC were abolished by pre-treatment with (2S)-2-amino-2[(1S,2S)-2-carboxycycloprop-1-yl]-3-(xanth-9-yl) propanoic acid (LY341495), a group II mGluR antagonist. These results indicate that peripheral group II mGluRs are involved in the development and maintenance of IL-1beta-induced mechanical allodynia, while peripheral group I mGluRs are involved in the development of IL-1beta-induced mechanical allodynia. Based on our observations, the peripheral application of group II mGluR agonists may be of therapeutic value in treating inflammatory pain.

Received May 18, 2015 Revised July 10, 2015 Accepted July 20, 2015 Address for correspondence SungHee Kim, MD, PhD Department of OtolaryngologyHead and Neck Surgery, Daegu Fatima Hospital, 99 Ayang-ro, Dong-gu, Daegu 41199, Korea Tel +82-53-940-7350 Fax +82-53-940-7352 E-mail sungheekim@fatima.or.kr Background and ObjectivesZZBone conduction (BC) auditory brainstem response (ABR) is an important factor in determining the type of hearing loss especially in infants and other difficult-to-test populations. However, multiple constraints including technical difficulties make evaluating BC ABR less feasible in the clinic, and there is also lack of information that guides clinicians how to evaluate it. The purpose of this study is to compare the latency of wave V in BC and air conduction (AC) ABR in normal hearing infants and gather reference values for wave V latency of BC ABR. Subjects and MethodZZA total of 210 ears of normal hearing, of those not belong to the hearing loss risk group, were included. All the infants underwent ABR evoked by clicks via AC (3A insert phone) and BC (Radioear B-71, vibrator positioned on the mastoid) under sedation. The latency of wave V at 30 dB nHL by BC and AC was compared and analyzed according to age. ResultsZZThe results revealed that in every age group in the study, wave V latency at 30 dB nHL of BC ABR was shorter than that of AC ABR. There was a significant decrease in BC and AC latencies with age, but among each consecutive age group, significant latency change was not identified after 6 months old. ConclusionZZThe latency of BC ABR in young children was shorter than that of AC ABR, and it decreased significantly as age increased. However, the reference data should be considered by taking each laboratory’s test parameter into consideration. Korean J Otorhinolaryngol-Head Neck Surg 2015;58(10):676-81

Spontaneous nystagmus is a reflection of tonic left-right vestibular asymmetry. It is typically seen after a recent unilateral peripheral vestibular lesion and has fast phases away from the side of the lesion. Sometimes spontaneous nystagmus is seen in the absence of a recent unilateral peripheral lesion, in which case it provides evidence of a vestibular lesion but does not localize it. We experienced a case of 35-year-old man who had sudden sensorineural hearing loss on the left side with acute onset of vertigo and transient spontaneous nystagmus, which had fast phases away from the side of the sudden deafness, without canal paresis on the bithermal caloric test.� Korean J Otorhinolaryngol-Head Neck Surg 2012;55:578-81 Key WordsZZCaloric tests ㆍSpontaneous ocular nystagmus ㆍSudden hearing loss ㆍVertigo.

Purpose: The purpose of this study was to compare knowledge level of those clinical nurses’ who received HPV vaccine and those who did not and their perception of the relatedness of HPV vaccine to causes of cervical cancer. Methods: A total of 249 clinical nurses were surveyed from June to July, 2009. The questionnaire originally developed by Kim & Ahn (2007) examined HPV-related knowledge originally and the tool for perception of the causes of cervical cancer was originally developed by Kim (1992). The total number of subjects equaled to: vaccination group of 52 (20.9%) and non-vaccination group of 197 (79.1%). Results: Vaccination group showed significantly higher score of both knowledge of HPV vaccination and the perception of the cause of cervical cancer in comparison to the nonvaccination group at (p

Synthetic oligodeoxynucleotides (ODN) with a CpG-motif are recognized by Toll-like receptor 9 (TLR9) and pleiotropic immune responses are elicited. Stimulation of macrophages with TLR9 agonist prevented apoptosis induced by serum deprivation through increased expression of FLICE-like inhibitory protein (FLIP). CpG ODN-mediated anti-apoptosis depended on the TLR9-Akt-FoxO3a signaling pathway. Inhibition of TLR9 by small interfering (si) RNA or an inhibitor suppressed CpG ODN-mediated anti-apoptosis. Analysis of signaling pathways revealed that the anti-apoptotic effect of CpG ODN required phosphorylation of FoxO3a and its translocation from the nucleus to the cytosol. Overexpression of FoxO3a increased apoptosis induced by serum deprivation and CpG ODN blocked these effects through FLIP expression. In contrast, siRNA knock-down of FoxO3a decreased apoptosis by serum deprivation. In addition, Akt activation was involved in CpG ODN-induced phosphorylation of FoxO3a, expression of FLIP, and anti-apoptosis. Taken together, these results demonstrate the involvement of Akt-FoxO3a in TLR9-mediated anti-apoptosis and indicate that FoxO3a is a distinct regulator for FLIP expression.

Background and Objectives：In this study, we evaluated the effect of bimodal hearing in the speech perception test and the increasing level of bimodal hearing over cochlear implantation in speech perception score regarding residual hearing. Subjects and Method：Nineteen prelingually deaf patients, who had used bimodal hearing over a period of 8 months, were divided in two groups in accordance to their low frequency residual hearing. The children were tested in open-set speech perception under +10 SNR and +20 SNR. The scores of bimodal hearing and unilateral cochlear implantation were compared by the Wilcoxon signed-rank test. Also, the increased level of speech perception scores of bimodal hearing over cochlear implantation alone were calculated using the formula, [bimodal score (%) - unilateral cochlear implantation (%)], and was compared between groups. Results：In pure tone audiometry under silent condition, the result of bimodal hearing was similar to unilateral cochlear implantation in magnitude in both groups. Under the noisy condition, both groups had better result in bimodal hearing in terms of speech perception. Also, the increased level was higher in bimodal hearing over unilateral cochlear implantation in the better residual hearing group. However, since the sample size was small enough, it is considered that there was no statistical significance. Conclusion：Cochlear implanted patients with residual hearing are expected to get better speech perception in noisy environment with bimodal hearing regardless of the level of residual hearing. (Korean J Otorhinolaryngol-Head Neck Surg 2009;52:29-35)

Background and Objectives：Among inner ear anomaly, incomplete partition type III is a quite rare finding which has pathognomonic computerized tomographic finding with bilateral, dilatation of lateral end of internal auditory canal, and deficient or absent bone between internal auditory canal and the basal turn of cochlea. Patients with incomplete partition type III have various range of hearing impairment and in case of severe hearing loss which cannot get benefit from hearing aids, cochlear implantation is indicated. In cochlear implantation for incomplete partition type III, perilymph gusher and abnormal electrode position is highly cautioned. We analyzed cochlear implantation patients with incomplete partition type III to find common intra-operative finding and complication. Subjects and Method：Temporal bone computerized tomographies of 120 patients who received cochlear implantation between September, 2002 and March, 2008 in our hospital were reviewed：the imaging of 4 patients were consistent with typical incomplete partition type III. We reviewed intra-operative finding and postoperative complications along with hearing outcome. Results：During the operation, perilymph gusher was encountered in all cases, and it was tightly sealed with subcutaneous tissue and fat with fibrin glue. In patient 1, electrodes were abnormally positioned in IAC causing facial nerve stimulation. However, the result of postoperative speech perception was good in the patient, and in the rest of patients, the results were various. Conclusion：The surgeon should be aware of perilymph gusher when cochlear implantation is performed on patients with characteristic temporal bone computerized tomographic findings and who are suspicious of incomplete partition type III. (Korean J Otorhinolaryngol-Head Neck Surg 2009;52:492-7)

The azimuthal anchoring energies (A.A.E.) of rubbed and UV-exposed polyimides (PIs) alignment layers were measured more precisely by using improved optical measurement systems and modified cell configurations, and their effects on the alignment stabilities and liquid crystal (LC) response properties in an IPS-mode LCD were studied. It is proved that (1) the relatively high A.A.E. is necessary for the alignment stability under high temperature stresses, and (2) the falling time of LC becomes shorter by about 0.7 ms with one order increase of an A.A.E. value. So we propose that the A.A.E. level of 1 × 10−2 ∼ 5 × 10−2 J/m2 is required for an alignment layer in an IPS-mode LCD in order to guarantee the alignment stability and LC response property.