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Objective. Untreated obstructive sleep apnea syndrome (OSAS) increases the risk of cardiovascular, dementia, and motor vehicle accident events. However, continuous positive airway pressure (CPAP) which is the gold standard treatment is not acceptable for many patients with OSAS. Development of devices for the patients of nonadherence to CPAP is necessary. Materials and Methods. We evaluated the effect of the smart antisnore pillow (SAP) in patients with OSAS in a prospective, noncontrolled, nonrandomized, pilot study. According to the apnea-hypopnea index (AHI), they were divided into two groups: mild-to-moderate OSAS group and severe OSAS group. Single-night polysomnography (PSG) with application of a SAP was performed. Thirty patients, 15 males and 15 females, 33–82 years old (mean age, 59.3 ± 12.9 years), completed the smart antisnore pillow therapy test. Among them, 23 patients had mild-to-moderate OSAS. Results. The SAP significantly improved the snore number ( p = 0.018 ), snore index ( p = 0.013 ), oxygen denaturation index ( p = 0.001 ), total AHI ( p = 0.002 ), and supine AHI ( p = 0.002 ) in the mild-to-moderate OSAS group, but there was no significant improvement in the severe OSAS group. Conclusions. We concluded that the SAP is an effective positional therapy device for patients with OSAS of mild-to-moderate severity.

Tricetin is a flavonoid derivative and a potent anti-inflammatory and anticancer agent. However, the molecular mechanism underlying the effects of tricetin on human oral cancer cell migration remains unclear. The cell migration and invasion abilities of three oral cancer cell lines (SCC-9, HSC-3, and OECM-1) were analyzed using Boyden chamber migration assays. Our results demonstrated that tricetin attenuates 12-O-tetradecanoylphorbol-13-acetate-induced SCC-9, HSC-3, and OECM-1 cell invasiveness and migration by reducing matrix metalloproteinase (MMP)-9 enzyme activity. The reverse transcription polymerase chain reaction and luciferase reporter assay revealed that tricetin downregulates the mRNA expression and promoter activity of MMP-9. In addition, Western blot analysis revealed that tricetin significantly reduced the levels of phosphorylated c-Jun N-terminal kinase (JNK) 1/2 and p38 levels but not those of extracellular signal-regulated kinase 1/2. In conclusion, this study demonstrated that tricetin suppresses MMP-9 enzymatic activity by downregulating the p38/JNK1/2 pathway and might be a beneficial chemopreventive agent.

Summary The purpose of this study was to investigate the impact of MCP-1 and its receptor CCR2 gene polymorphisms on the susceptibility and clinicopathological characteristics of oral cancer, as well as the synergistic effect between these gene polymorphisms and well-known risk factors including alcohol, tobacco, and areca consumptions. Using polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP) technique for polymorphism analysis, 344 healthy controls and 216 oral cancer patients were recruited to reveal a significant association between V64I CCR2 gene polymorphism and oral cancer susceptibility. After adjusting for other confounders, individuals with GA (AOR = 1.84; 95%CI = 1.10–3.20) or at least one A allele (AOR = 1.78; 95%CI = 1.05–3.02) had a higher risk for oral cancer, compared to GG genotypes. Moreover, results also revealed that for subjects with GA or at least one A allele of V64I CCR2 gene polymorphism, those exposed to environmental risk factors possessed a significantly higher risk for oral cancer than those unexposed subjects. Therefore, genetic polymorphism of CCR2-64I may contribute to the susceptibility to oral cancer.

Background This study investigates the association between polymorphism in the E-cadherin/CDH1 promoter region and the risk and progression of oral cancer. Methods Genetic polymorphisms of CDH1-160 and -347 were analyzed by polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) in 347 noncancer controls and in 251 patients with oral cancer. Results The statistical analysis showed that subjects with at least 1 varied GA allele of CDH1-347 polymorphic genotypes or combinations of the CDH1-160 CA/-347 GGA, CDH1-160 CC/-347 GGA, or CDH1-160 CC/-347 GAGA genotypes had a significantly higher risk, whereas subjects with CDH1-160 C/A or A/A had a significantly lower risk of developing oral cancer than those with wild-type genotypes. Furthermore, elderly patients with the CDH1-347 G/GA or GA/GA genotype were associated with a higher incidence in lymph node metastasis than were those with the G/G genotype. Conclusions These results suggest that CDH1-347 polymorphisms are associated with increased risks of oral cancer, and may be a predictive factor for tumor lymph node metastasis. © 2011 Wiley Periodicals, Inc. Head Neck, 2012

The levels of urokinase plasminogen activator (uPA) system in tumor tissues are implicated as prognostic biomarkers in a wide range of malignancies. However, their possible impact on the risk and prognosis of oral cancer and the susceptibility of environmental carcinogens to oral cancer remains poorly investigated. The genetic polymorphisms of uPA, uPA receptor (uPAR), and plasminogen activator inhibitor (PAI)-1 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 253 patients with oral cancer and 344 healthy controls. There was no significant effect of uPA system genes on the susceptibility of oral cancer; however, the impact of uPA system gene polymorphisms on the susceptibility of betel nut and tobacco consumptions to oral cancer was revealed, except for that of uPAR gene polymorphism on tobacco consumption. Patients with oral cancer with at least one 5G allele of PAI-1 gene have a low risk for the development of clinical stage III or IV (p ≤ 0.05) and lymph node metastasis (p ≤ 0.05) compared with those with 4G/4G homozygotes. Our results suggest that the combination of uPA system gene polymorphisms and environmental carcinogens was related to the risk of oral cancer, and the genetic polymorphism of PAI-1 was associated with a low risk to the clinicopathological development of oral cancer.

Oral squamous cell carcinoma has a striking tendency to migrate and metastasize. Cyclooxygenase (COX)-2, the inducible isoform of prostaglandin (PG) synthase, has been implicated in tumor metastasis. However, the effects of COX-2 on human oral cancer cells are largely unknown. We found that overexpression of COX-2 or exogenous PGE(2) increased migration and intercellular adhesion molecule 1 (ICAM)-1 expression in human oral cancer cells. Using pharmacological inhibitors, activators, and genetic inhibition of EP receptors, we discovered that the EP1 receptor, but not other PGE receptors, is involved in PGE(2)-mediated cell migration and ICAM-1 expression. PGE(2)-mediated migration and ICAM-1 up-regulation were attenuated by inhibitors of protein kinase C (PKC)δ, and c-Src. Activation of the PKCδ, c-Src, and AP-1 signaling pathway occurred after PGE(2) treatment. PGE(2)-induced expression of ICAM-1 and migration activity were inhibited by a specific inhibitor, siRNA, and mutants of PKCδ, c-Src, and AP-1. In addition, migration-prone sublines demonstrated that cells with increased migration ability had higher expression of COX-2 and ICAM-1. Taken together, these results indicate that the PGE(2) and EP1 interaction enhanced migration of oral cancer cells through an increase in ICAM-1 production.

Background The internal carotid artery, the internal jugular vein, and the spinal accessory nerve are the main structures that are preserved in conservative neck dissections. In the upper neck, one surgical landmark used to find these structures is the transverse process of a cervical vertebral body. There is controversy about the origin of the transverse process in the upper neck. Methods We applied three-dimensional computerized tomography (3-D CT), an intraoperative navigational system and cadaver dissection of the neck to clarify the controversy. Results The origin of the transverse process was from the atlas (C1). Conclusions The transverse process of the atlas is an important surgical landmark in the upper neck. The neurovascular bundle is located anteriorly. The transverse process of the axis (C2) is less prominent and is situated antero-inferior to the spinal accessory nerve where the nerve emerges from the posterior border of the internal jugular vein. © 1997 John Wiley & Sons, Inc. Head Neck 19: 37–40, 1997.

Oral cancer is the fourth common male cancer and causally associated with environmental carcinogens in Taiwan. The reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) has a significant effect on tumorigenesis by limiting angiogenesis and invasion of tumors through the extracellular matrix. RECK downregulation has been confirmed in many human cancers and associated with lymph node metastasis clinically. In the present hospital-based case-controlled study, the demographic, RECK genotype and clinicopathologic data from 341 male oral cancer patients and 415 cancer-free controls were investigated. We found that RECK rs10814325, rs16932912, rs11788747 or rs10972727 polymorphisms were not associated with oral cancer susceptibility. Among 488 smokers, RECK polymorphisms carriers with betel quid chewing have a 7.62-fold [95% confidence interval (CI), 2.96-19.64] to 25.33-fold (95% CI, 9.57-67.02) risk to have oral cancer compared with RECK wild-type carrier without betel quid chewing. Among 352 betel quid chewers, RECK polymorphisms carriers with smoking have a 6.68-fold (95% CI, 1.21-36.93) to 18.57-fold (95% CI, 3.80-90.80) risk to have oral cancer compared with those who carried wild-type without smoking. In 263 betel quid chewing oral cancer patients, RECK rs10814325 polymorphism have a 2.26-fold (95% CI, 1.19-4.29) risk to have neck lymph node metastasis compared with RECK wild-type carrier. These results support that gene-environment interactions between the RECK polymorphisms, smoking and betel quid may alter oral cancer susceptibility and metastasis.

Background The purpose of this study was to evaluate the influence of genetic polymorphisms of interleukin (IL)-23 and the IL-23 receptor (IL-23R) on the susceptibility to oral cancer. Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to measure polymorphisms of these genes in 240 controls and 240 patients with oral cancer. Results Individuals with at least 1 varied C allele of rs10889677 (IL-23R polymorphism) had a 1.553-fold risk (95% confidence interval [CI], 1.073–2.241) of developing oral cancer compared with patients with the wild-type A/A homozygote. Patients with oral cancer with at least 1 varied C allele of rs10889677 had a 1.931-fold risk of tumor lymph node metastasis compared with patients with the C/C homozygote. Conclusion The varied C allele of the IL-23R gene may be considered a factor contributing to increased susceptibility and may be a predictive factor for tumor lymph node metastasis in Taiwanese with oral cancer. © 2011 Wiley Periodicals, Inc. Head Neck, 2012

Matrix metalloproteinase (MMP)-14 is one of the pericellular collagenases to degrade extracellular matrix (ECM), which is involved to the modulation of susceptibility or clinicopathological features of a cancer. The contributions of MMP-14 on the susceptibility or clinicopathological features of certain cancers have been well documented, and the expression of MMP-14 in oral squamous cell carcinoma (OSCC) also has been observed. This study was designed to examine the association of MMP-14 gene polymorphisms with the susceptibility and clinicopathological development of OSCC.A total of 363 patients with OSCC and 506 healthy control subjects were recruited. Six single nucleotide polymorphisms (SNPs) of MMP-14 genes were analyzed by polymerase chain reaction-restriction fragment length polymorphism genotyping and haplotype-base analysis.MMP-14 +7096 TC/CC genotypes might lower the risk of OSCC, and MMP-14 +6767 GA/AA genotypes cause a poor clinical status in OSCC patients. The +6727 C: +6767 G: +7096 T: +8153 G haplotype and diplotype increased the risk for OSCC by 1.706-fold (95% confidence interval (CI) 1.383-2.105) and 2.276-fold (95% CI = 1.531-3.384), respectively, compared with the reference. The diplotype with at least one CGTG exhibited a high risk (adjusted odds ratio, 1.639; 95% CI, 1.005-2.673) for developing a poor clinicopathological diagnosis of OSCC compared with the others/other diplotype.The +7096 and +6767 polymorphic genotypes and haplotype +6727 C: +6767 G: +7096 T: +8153 G of MMP-14 gene might contribute to the prediction of susceptibility and pathological development of OSCC.

Inflammation can be induced by cytokines, chemokines, and their receptors, and it is believed to be a risk factor on tumor initiation and progression. The contribution of CC chemokine ligand 5 (CCL5) and CC chemokine receptor 5 (CCR5) on the risk and prognosis of oral cancer is still poorly investigated. The aims of this study were to investigate the impacts of single nucleotide polymorphisms (SNPs) in CCL5 and CCR5 genes and the synergistic effects of these SNPs on the risk and clinicopathological characteristics of oral cancer. In this case-control study, a total of 253 oral cancer patients and 347 controls were recruited. The genetic polymorphisms of CCL5-28, -403 and CCR5-59029 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping analysis. The results of statistical analysis showed that the subjects with CCL5-28 CG, CCL5-28 CG or GG, and CCL5-403 TT polymorphic genotype as well as the subjects with the combinations of CCL5-28 CG/-403 CT and CCL5-28 CG/-403 TT genotypes having a significant higher risk to oral cancer than those with wild-type genotypes. Moreover, the oral cancer patients with the combination of CCL5-28 CG/-403 TT genotype presented a lower risk for developing a moderately or poorly differentiated status as compared to those with the combination of CCL5-28 CC/-403 CC genotype. These results suggest that the SNPs in CCL5-28 and -403 genes could increase the risk to have oral cancer, and the combinative effect of CCL5-28 CG and -403 TT genes might also increase the oral cancer risk but reduce the clinicopathological development of oral cancer patients.

Background. The aim of this study was to estimate the relationship of glutathione S-transferases (GST)P1, GSTA1, GSTM1, and GSTT1 gene polymorphisms to oral cancer risk. Methods. Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) was used to measure these 4 gene polymorphisms in 274 controls and 164 oral cancer patients. Results. Individuals with at least 1 varied G allele of GSTP1 had a 1.53-fold risk (95% confidence interval [CI] = 1.01–2.31) of developing oral cancer compared with patients with wild-type A/A homozygotes. Oral cancer patients with at least 1 varied T allele of GSTA1 gene had a 0.42-fold risk (95% CI = 0.18–0.95) of having a tumor size >2 cm compared with patients with C/C homozygotes. Conclusions. The varied G allele of GSTP1 may be considered as a factor contributing to increased susceptibility, whereas the T allele of GSTA1 could be a protective factor for tumor size progression in Taiwanese with oral cancer. © 2009 Wiley Periodicals, Inc. Head Neck, 2010

The aim of this study was to estimate the relations between hypoxia inducible factor-1alpha (HIF-1alpha) gene polymorphisms, C1772T and G1790A, to the susceptibility and clinicopathological status of oral cancer. A total of 521 subjects, including 347 controls and 174 oral cancer patients, were recruited in this study and subjected to polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) to analyze the impact of these two polymorphic variants on oral cancer. A significant association between oral cancer susceptibility and G1790A polymorphism was demonstrated since individuals with heterozygotes, that is GA, had a higher risk for oral cancer, compared to GG genotypes after adjusting for other confounders (AOR=3.31; 95%CI=1.27-8.61). Compared to individuals with both C1772C and G1790G homozygotes, individuals with at least one of either C1772T or G1790A of HIF-1alpha gene had a risk of 2.17-folds (95% CI=1.0-4.75) to develop oral cancer. Moreover, results also revealed the presence of synergistic effect between gene polymorphisms of HIF-1alpha and environmental risk factors, such as tobacco and betel nut consumptions while there was no significant association between HIF-1alpha gene polymorphism and clinicopathological parameters of oral cancer. Genetic polymorphism, including C1772T and G1790A, of HIF-1alpha is an important factor for the susceptibility to oral cancer.

The aim of this study was to evaluate the relations of SDF-1 and its receptor, CXCR4, gene variants on oral cancer risk.PCR-RFLP was used to measure SDF-1-3'A and CXCR4 gene polymorphisms in 284 controls and 113 patients with oral cancer.After being adjusted for age, individuals with A/G heterozygotes of SDF-1 had a higher risk of 1.86-fold to develop oral cancer when compared with those with G/G wild type homozygotes. Furthermore, patients with oral cancer with at least 1 mutant T allele of CXCR4 gene had a risk of 2.66-fold to progress to stage III or IV.SDF-1-3'A gene polymorphism may be considered as a factor of increased susceptibility to oral cancer, and at least 1 mutated T allele of CXCR4 gene is associated with the development of stage III or IV and the induction of lymph-node metastasis of oral cancer disease in Taiwanese.

The authors have designed a method of reconstruction for high pharyngeal and oesophageal defects that potentially avoids many of the disadvantages related to size mismatch at the proximal and distal end of oesophageal defects that are encountered with the use of free jejunal and colon flaps, respectively. An ileo-colon flap was used to reconstruct this type of defect where the ascending colon was anastomosed to the pharyngeal end and the ileum was anastomosed to the oesophageal end. Both sides were perfectly matched in circumference and minimal manipulation was necessary at both ends of the flap. A detailed description of the surgical technique is depicted and a case presented. While this procedure solves some of the problems encountered when dealing with this type of defect, it nevertheless does have some disadvantages and technical nuisances that are detailed and discussed in this report.

BACKGROUND: The reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) down-regulation has been confirmed in numerous human cancers and is clinically associated with metastasis. This study investigates the potential associations of RECK single-nucleotide polymorphisms (SNPs) with hepatocellular carcinoma (HCC) susceptibility and its clinicopathologic characteristics. METHODOLOGY/PRINCIPAL FINDINGS: A total of 135 HCC cancer patients and 501 cancer-free controls were analyzed for four RECK SNPs (rs10814325, rs16932912, rs11788747, and rs10972727) using real-time PCR and PCR-RFLP genotyping analysis. After adjusting for other co-variants, the individuals carrying RECK promoter rs10814325 inheriting at least one C allele had a 1.85-fold [95% confidence interval (CI), 1.03-3.36] risk of developing HCC compared to TT wild type carriers. The HCC patients, who carried rs11788747 with at least one G allele, had a higher distant metastasis risk than wild type probands. CONCLUSIONS: RECK gene polymorphisms might be a risk factor increasing HCC susceptibility and distant metastasis in Taiwan.

The prevalence of the Epstein-Barr virus (EBV) Taiwan variant was investigated in the throat washing (TW) samples from patients with head and neck tumors, persons with nonmalignant diseases, and healthy adults in Taiwan. By using the EBV (BNLF-1 gene)-specific primers and PCR, the EBV latent membrane protein gene BNLF-1 was detected in 91 (61%) of the 150 TW samples from patients with tumors, including 25 (78%) of 32 patients with nasopharyngeal carcinoma and 66 (56%) of 118 other patients with head and neck tumors. The TW samples from the 26 patients with nonmalignant tumors and 53 healthy adults were also examined. Approximately 47% of these samples were positive for the EBV gene. The PCR products of the BNLF-1 gene were then subjected to XhoI digestion. Sixty-eight of 91 PCR products (75%) showed the loss of the XhoI site, which indicated the presence of a Taiwan strain of EBV in patients with tumors. The DNA sequence of the BNLF-1 gene of the Taiwan variant revealed that the loss of the XhoI site was due to a nucleotide change from a G to a T at position 169,426 in comparison with the sequence of prototype EBV B95-8 cells. Furthermore, the Taiwan strain appeared significantly more frequently in the TWs and tissue samples from patients with nasopharyngeal carcinoma (88%; P < 0.001) and laryngeal carcinoma (80%; P < 0.02) than in those samples from healthy adults (about 40%). These data indicate that a Taiwan variant of EBV may be closely associated with head and neck tumors and suggest that this variant may be important in the pathogenesis of head and neck tumors.