Identification and validation of the clinical prediction model and biomarkers based on chromatin regulators in colon cancer by integrated analysis of bulk- and single-cell RNA sequencing data.

Background: Chromatin regulators (CRs) are implicated in the development of cancer, but a comprehensive investigation of their role in colon adenocarcinoma (COAD) is inadequate. The purpose of this study is to find CRs that can provide recommendations for clinical diagnosis and treatment, and to explore the reasons why they serve as critical CRs. Methods: We obtained data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Weighted Gene Co-Expression Network Analysis (WGCNA) screened tumor-associated CRs. LASSO-Cox regression was used to construct the model and to screen key CRs together with support vector machine (SVM), the univariate Cox regression. We used single-cell data to explore the expression of CRs in cells and their communication. Immune infiltration, immune checkpoints, mutation, methylation, and drug sensitivity analyses were performed. Gene expression was verified by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Pan-cancer analysis was used to explore the importance of hub CRs. Results: We finally obtained 32 tumor-associated CRs. The prognostic model was constructed based on RCOR2, PPARGC1A, PKM, RAC3, PHF19, MYBBP1A, ORC1, and EYA2 by the LASSO-Cox regression. Single-cell data revealed that the model was immune-related. Combined with immune infiltration analysis, immune checkpoint analysis, and tumor immune dysfunction and exclusion (TIDE) analysis, the low-score risk group had more immune cell infiltration and better immune response. Mutation and methylation analysis showed that multiple CRs may be mutated and methylated in colon cancer. Drug sensitivity analysis revealed that the low-risk group may be more sensitive to several drugs and PKM was associated with multiple drugs. Combined with machine learning, PKM is perhaps the most critical gene in CRs. Pan-cancer analysis showed that PKM plays a role in the prognosis of cancers. Conclusions: We developed a prognostic model for COAD based on CRs. Increased expression of the core gene PKM is linked with a poor prognosis in several malignancies.

Construction of magnetic drug delivery system and its potential application in tumor theranostics.

Magnetic nanoparticles(NPs) are characterized by a rich variety of properties. Because of their excellent physical and chemical properties, they have come to the fore in biomedicine and other fields. The magnetic NPs were extensively studied in magnetic separation of cells, targeted drug delivery, tumor hyperthermia, chemo-photothermal therapy, magnetic resonance imaging (MRI) and other biomedical fields. Magnetic NPs are increasingly used in magnetic resonance imaging (MRI) based on their inherent magnetic targeting, superparamagnetic enzyme-like catalytic properties and nanoscale size. Poly(lactic-co-glycolic acid) (PLGA) is a promising biodegradable material approved by FDA and EU for drug delivery. Currently, PLGA-based magnetic nano-drug delivery systems have attracted the attention of researchers. Herein, we achieved the effective encapsulation of sized-controlled polyethylene glycol-3,4-dihydroxy benzyl-amine-coated superparamagnetic iron oxide nanoparticles (SPIO NPs) and euphorbiasteroid into PLGA nanospheres via a modified multiple emulsion solvent evaporation method (W1/O2/W2). NPs with narrow size distribution and acceptable magnetic properties were developed that are very useful for applications involving cancer therapy and MRI. Furthermore, SPIO-PLGA NPs enhanced the MRI T2 relaxation properties of tumor sites.The prepared SPIO NPs and magnetic PLGA nanospheres can be promising magnetic drug delivery systems for tumor theranostics. This study has successfully constructed a tumor-targeting and magnetic-targeting smart nanocarrier with enhanced permeability and retention, multimodal anti-cancer therapeutics and biodegradability, which could be a hopeful candidate for anti-tumor therapy in the future.

Correction: PSC-derived Galectin-1 inducing epithelial-mesenchymal transition of pancreatic ductal adenocarcinoma cells by activating the NF-κB pathway.

[This corrects the article DOI: 10.18632/oncotarget.21212.].

Ligand-modified homologous targeted cancer cell membrane biomimetic nanostructured lipid carriers for glioma therapy.

The main treatment measure currently used for glioma treatment is chemotherapy; the biological barrier of solid tumors hinders the deep penetration of nanomedicines and limits anticancer therapy. Furthermore, the poor solubility of many chemotherapeutic drugs limits the efficacy of antitumor drugs. Therefore, improving the solubility of chemotherapeutic agents and drug delivery to tumor tissues through the blood-brain barrier (BBB) and blood-brain tumor barrier (BBTB) are major challenges in glioma treatment. Nanostructured lipid carriers (NLCs) have high drug loading capacity, high stability, and high in vivo safety; moreover, they can effectively improve the solubility of insoluble drugs. Therefore, in this study, we used solvent volatilization and ultrasonic melting methods to prepare dihydroartemisinin nanostructured lipid carrier (DHA-NLC). We further used the glioma C6 cancer cell (CC) membrane to encapsulate DHA-NLC owing to the homologous targeting mechanism of the CC membrane; however, the targeting ability of the CC membrane was weak. We accordingly used targeting ligands for modification, and developed a bionanostructured lipid carrier with BBB and BBTB penetration and tumor targeting abilities. The results showed that DHA-loaded NGR/CCNLC (asparagine-glycine-arginine, NGR) was highly targeted, could penetrate the BBB and BBTB, and showed good anti-tumor effects both in vitro and in vivo, which could effectively prolong the survival time of tumor-bearing mice. Thus, the use of DHA-loaded NGR/CCNLC is an effective strategy for glioma treatment and has the potential to treat glioma.

[Balloon Eustachian tuboplasty for treatment of Eustachian tube dysfunction: A systematic review and Meta-analysis].

Objective:To sysetematically evaluate the efficacy, compliance and collaborative operation of Balloon Eustachian tuboplasty（BET） for treatment of Eustachian tube dysfunction via Meta-analysis. Method:The PubMed, OVID, Embase, Cochrane Library, ProQuest, Web of Science, Chinese biomedical literature database, VIP database, WanFang database, CNKI were searched for papers on autoinflation for treatment of chronic otitis media with effusion in children（up to March 2020）. Statistical analysis was performed by using Cochrane tools and RevMan5.2. Result:A total of 14 articles were included. The results of Meta-analysis showed that the effective rate of the BET was 86%（95%CI: 0.79-0.94）, and had statistical significance. The tubomanometry, ETS, ETDQ-7 of postoperative BET was better than that of the control group, and had statistical significance. Heterogeneity of tubomanometry,ETS was relatively small, which is I²=51%（OR 3.57, 95%CI ：1.95 - 6.55） and I²=59%（SMD 1.33, 95%CI ：0.98-1.67） respectively. There was no statistical significance between BET plus tympanic paracentesis compared with those treated with BET alone. The recurrence rate of the included literature was 5.37% and the complication rate was only 0.33%. Conclusion:Balloon Eustachian tuboplastycan be a safe and effective treatment for adult Eustachian tube dysfunction. However, in terms of collaborative surgery and evaluation methods, we still need more homogeneous, multi-center randomized controlled studies to obtain more accurate conclusions to guide clinical practice.

Intestinal microbiota: a new force in cancer immunotherapy.

Cancer displays high levels of heterogeneity and mutation potential, and curing cancer remains a challenge that clinicians and researchers are eager to overcome. In recent years, the emergence of cancer immunotherapy has brought hope to many patients with cancer. Cancer immunotherapy reactivates the immune function of immune cells by blocking immune checkpoints, thereby restoring the anti-tumor activity of immune cells. However, immune-related adverse events are a common complication of checkpoint blockade, which might be caused by the physiological role of checkpoint pathways in regulating adaptive immunity and preventing autoimmunity. In this context, the intestinal microbiota has shown great potential in the immunotherapy of cancer. The intestinal microbiota not only regulates the immune function of the body, but also optimizes the therapeutic effect of immune checkpoint inhibitors, thus reducing the occurrence of complications. Therefore, manipulating the intestinal microbiota is expected to enhance the effectiveness of immune checkpoint inhibitors and reduce adverse reactions, which will lead to new breakthroughs in immunotherapy and cancer management. Video abstract.

Clinical nomogram for lymph node metastasis in pathological T1 esophageal squamous cell carcinoma: a multicenter retrospective study.

BACKGROUND: Endoscopic resection is increasingly used to treat pathological T1 (pT1) esophageal cancer (EC) patients. However, the procedures are limited by lymph node metastasis (LNM) and remain controversial. We aimed to construct a nomogram to predict the risk of LNM in patients with pT1 esophageal squamous cell carcinoma (ESCC). METHODS: A total of 243 patients with pT1 ESCC who underwent esophagectomy and lymph node dissection at two different institutes between February 2013 and June 2019 were analyzed retrospectively. Patients were categorized into the negative group and the positive group according to whether there was LNM. Risk factors for LNM were evaluated by univariate and multivariate analyses. The nomogram was used to estimate the individual risk of LNM. RESULTS: Forty-six (18.9%) of the 243 patients with pT1 ESCC exhibited LNM. The LNM rate in patients with stage T1a disease was 5.7% (5/88), and the rate in patients with stage T1b disease was 26.5% (41/155). Multivariable logistic regression analysis showed that tumor differentiation [odds ratio (OR) =1.942, 95% confidence interval (CI): 1.067-3.536, P=0.030], the T1 sub-stage (OR =4.750, 95% CI: 1.658-13.611, P=0.004), the preoperative alanine aminotransferase/aspartate aminotransferase ratio (LSR) (OR =5.371, 95% CI: 1.676-17.210, P=0.005), and the high-density lipoprotein cholesterol (HDL-C) level (OR =5.894, 95% CI: 1.917-18.124, P=0.002) were independent risk factors for LNM. The nomogram had relatively high accuracy, with an area under the receiver operating characteristic curve (AUC) of 0.803 (95% CI: 0.732-0.873). The calibration curve showed that the predicted probability of LNM was in good agreement with the actual probability. CONCLUSIONS: Clinicopathological and hematological parameters of tumor differentiation, the T1 sub-stage, the preoperative LSR, and the HDL-C level may predict the risk of LNM in T1 ESCC. The risk of LNM can be predicted by the nomogram.

[Identification of SDHD c.170-1G>T variant in pedigree affected with carotid body tumor].

OBJECTIVE: To carry out genetic testing for a pedigree affected with carotid body tumor (CBT). METHODS: Members of the pedigree were enrolled and underwent physical examination, ultrasonography and CT scan. Genomic DNA of the proband was extracted from peripheral blood sample and subjected to exome sequencing. Candidate variants were predicted using bioinformatic tools and verified among members from his pedigree. RESULTS: A c.170-1G>T splicing variant of the SDHD gene was detected in 15 individuals from the pedigree. Physical examination and imaging confirmed that 9 of them had CBT and hypertension, while the remaining 6 died of cardiovascular and cerebrovascular diseases. CONCLUSION: The c.170-1G>T variant of the SDHD gene probably underlies the CBT in this pedigree. Genetic testing should be considered for CBT patients with CBT in addition to conventional clinical examination.

Clinical outcome and prognostic analysis of young adults nasopharyngeal carcinoma patients of a nonendemic area in intensity-modulated radiotherapy era.

AIM: To investigate the clinical outcome and prognostic factors of young adults nasopharyngeal carcinoma (NPC) patients in the era of intensity-modulated radiotherapy. METHODS: We retrospectively analyzed the clinical outcome and the prognostic factors of young adults NPC patients who were admitted to our hospital from January 2010 to December 2013. COX regression model was used to identify factors associated with survival. The acute and late toxicities were also evaluated. RESULTS: A total of 165 patients were included; the median follow-up time for all the patients was 65 months (4-96 months). The 5-year overall survival (OS), distant metastasis-free survival, progression-free survival and local-regional recurrence-free survival were 85.9, 82.4, 76.4 and 92.4%, respectively. N stage was an independent prognostic factor for OS (p = 0.009) and distant metastasis-free survival (p = 0.008). Cumulative cisplatin >200 mg/m2 was an independent prognostic factor for OS (p = 0.032). CONCLUSION: Young adults with NPC can achieve a reasonable local-regional control and OS in the era of intensity-modulated radiotherapy with tolerable toxicities.

The role of microbiota in the development of colorectal cancer.

Colorectal cancer is the third largest cancer in worldwide and has been proven to be closely related to the intestinal microbiota. Many reports and clinical studies have shown that intestinal microbial behavior may lead to pathological changes in the host intestines. The changes can be divided into epigenetic changes and carcinogenic changes at the gene level, which ultimately promote the production and development of colorectal cancer. This article reviews the pathways of microbial signaling in the intestinal epithelial barrier, the role of microbiota in inflammatory colorectal tumors, and typical microbial carcinogenesis. Finally, by gaining a deeper understanding of the intestinal microbiota, we hope to achieve the goal of treating colorectal cancer using current microbiota technologies, such as fecal microbiological transplantation.

Galectin-1 expression in activated pancreatic satellite cells promotes fibrosis in chronic pancreatitis/pancreatic cancer via the TGF-ß1/Smad pathway.

Chronic pancreatitis/pancreatic cancer (CP/PC) is characterized by fibrous connective tissue proliferation induced by activated pancreatic stellate cells (PSCs). Galectin-1 is upregulated in activated PSCs and is important for the continuing activation of PSCs. The aim of this study was to evaluate the effect of galectin-1 derived from activated PSCs on the progression of fibrosis in CP/PC. To this end, the expression of desmin, α-SMA, galectin-1, fibronectin and collagen type I in normal pancreatic, CP and PC tissues, as well as quiescent/activated PSCs, was investigated. The proliferation rate and migration ability of control, galectin-1-overexpressing and galectin-1-silenced PSCs were also evaluated, as well as the mRNA and protein expression of fibronectin, collagen type I, α-SMA, tissue inhibitors of metalloproteinases (TIMP)-1, MMP-2, Smad2 and TGF-ß1. Furthermore, the effect of adding a TGF-ß1 receptor inhibitor on the expression of these proteins was examined. The results revealed that the expression profile of desmin, α-SMA, galectin-1, fibronectin and collagen type I in the normal pancreas was similar to that of quiescent PSCs and the expression profile in CP/PC tissues was similar to that of activated PSCs. Furthermore, galectin-1-overexpressing PSCs exhibited a significantly higher proliferation rate and migration ability, while galectin-1-silenced PSCs exhibited a significantly lower proliferation rate and migration ability than the control PSCs. The expression of fibronectin, collagen type I, α-SMA, MMP-2 and TIMP-1 was also significantly higher in the galectin-1-overexpressing PSCs than the control PSCs and this effect was found to be mediated by the TGF-ß1/Smad pathway. The trends in the expression of these factors were reversed in the galectin-1-silenced PSCs. From these findings, it can be concluded that overexpression of galectin-1 promotes PSC activity (proliferation and migration) and stimulates fibrosis by increasing extracellular matrix synthesis and decreasing the MMP/TIMP ratio via the TGF-ß1/Smad pathway. Thus, galectin-1 may be a novel candidate for reversing or halting fibrosis progression in CP/PC.

Functions of pancreatic stellate cell-derived soluble factors in the microenvironment of pancreatic ductal carcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal forms of cancer with poor prognosis because it is highly resistant to traditional chemotherapy and radiotherapy and it has a low rate of surgical resection eligibility. Pancreatic stellate cells (PSC) have become a research hotspot in recent years, and play a vital role in PDAC microenvironment by secreting soluble factors such as transforming growth factor ß, interleukin-6, stromal cell-derived factor-1, hepatocyte growth factor and galectin-1. These PSC-derived cytokines and proteins contribute to PSC activation, participating in PDAC cell proliferation, migration, fibrosis, angiogenesis, immunosuppression, epithelial-mesenchymal transition, and chemoradiation resistance, leading to malignant outcome. Consequently, targeting these cytokines and proteins or their downstream signaling pathways is promising for treating PDAC.

PSC-derived Galectin-1 inducing epithelial-mesenchymal transition of pancreatic ductal adenocarcinoma cells by activating the NF-κB pathway.

Galectin-1 has previously been shown to be strongly expressed in activated pancreatic stellate cells (PSCs) and promote the development and metastasis of pancreatic ductal adenocarcinoma (PDAC). However, the molecular mechanisms by which Galectin-1 promotes the malignant behavior of pancreatic cancer cells remain unclear. In this study, we examined the effects of Galectin-1 knockdown or overexpression in PSCs co-cultured with pancreatic cancer (PANC-1) cells. Immunohistochemical analysis showed expression of epithelial-mesenchymal transition (EMT) markers and MMP9 were positively associated with the expression of Galectin-1 in 66 human PDAC tissues. In addition, our in vitro studies showed PSC-derived Galectin-1 promoted the proliferation, invasion, and survival (anti-apoptotic effects) of PANC-1 cells. We also showed PSC-derived Galectin-1 induced EMT of PANC-1 cells and activated the NF-кB pathway in vitro. Our mixed (PSCs and PANC-1 cells) mouse orthotopic xenograft model indicated that overexpression of Galectin-1 in PSCs significantly promoted the proliferation, growth, invasion, and liver metastasis of the transplanted tumor. Moreover, Galectin-1 overexpression in PSCs was strongly associated with increased expression of EMT markers in both the orthotopic xenograft tumor in the pancreas and in metastatic lesions of naked mice. We conclude that PSC-derived Galectin-1 promotes the malignant behavior of PDAC by inducing EMT via activation of the NF-κB pathway. Our results suggest that targeting Galectin-1 in PSCs could represent a promising therapeutic strategy for PDAC progression and metastasis.

[The clinical application of vestibular diagnosis and treatment system in benign paroxysmal positional vertigo].

OBJECTIVE: To evaluate the effect of the vestibular diagnosis and treatment system (SRM-IV ) in diagnosis and treatment of patients with benign paroxysmal positional vertigo (BPPV). METHOD: Patients who were diagnosed as BPPV by SRM-TV in the clinic of our hospital from November 2013 to October 2014 were retrospectively analyzed in this study. RESULT: Among 425 suspected cases, 230 BPPV-positive patients were diagnosed including 131 cases of posterior SC (57.0%), 95 cases of horizontal SC (41.3%) and 4 cases of more than two SC (1.7%). The cure rate by SRM-V was 94.6% and the effective rate was 100.0%. The relapsed occurred in 10 patients (4.8%), which contained 4 men and 6 women. CONCLUSION: SRM-V can realize 360° reasonable repositioning procedure while Canalish reposition procedure cannot. SRM-V can improve both the corrective rate of diagnosis and the cure rate, especially for the patients who suffered from complex BPPV.

Pancreatic satellite cells derived galectin-1 increase the progression and less survival of pancreatic ductal adenocarcinoma.

BACKGROUND: Galectin-1, a member of carbohydrate-binding proteins with a polyvalent function on tumor progression, was found strongly expressed in pancreatic satellite cells (PSCs), which partner in crime with cancer cells and promote the development of pancreatic ductal adenocarcinoma (PDAC). We evaluated the effects of PSCs derived Galectin-1 on the progression of PDAC, as well as the tumor establishment and development in mouse xenografts. METHODS: The relationship between immunohistochemistry staining intensity of Galectin-1 and clinicopathologic variables were assessed in 66 PDAC tissues, 18 chronic pancreatitis tissues and 10 normal controls. The roles of PSCs isolated from PDAC and normal pancreas on the proliferative activity, MMP2 and MMP9 expression, and the invasion of CFPAC-1 in the co-cultured system, as well as on the tumor establishment and development in mouse xenografts by mixed implanting with CFPAC-1 subcutaneously were evaluated. RESULTS: Galectin-1 expression was gradually increased from normal pancreas (negative), chronic pancreatitis (weak) to PDAC (strong), in which Galectin-1 expression was also increased from well, moderately to poorly differentiated PDAC. Galectin-1 staining intensity of pancreatic cancer tissue was associated with increase in tumor size, lymph node metastasis, perineural invasion and differentiation and UICC stage, and served as the independent prognostic indicator of poor survival of pancreatic cancer. In vitro and in vivo experiments indicated that TGF-ß1 upregulated Galectin-1 expression in PSCs, which could further promotes the proliferative activity, MMP2 and MMP9 expression, and invasion of pancreatic cancer cells, as well as the tumor establishment and growth. CONCLUSION: Galectin-1 expression in stromal cells of pancreatic cancer suggests that this protein plays a role in the promotion of cancer cells invasion and metastasis and provides a therapeutic target for the treatment of pancreatic cancer.

Long term results of pancreatectomy with portal-superior mesenteric vein resection for pancreatic carcinoma: a systematic review.

BACKGROUND/AIMS: Clinical benefit from pancreatectomy combined with portal vein/superior mesenteric resection in the pancreatic carcinoma with local venous invasion still remains controversial. The aim of this study was to review the overall outcome of the pancreatectomy combined with portal vein/superior mesenteric resection for pancreatic carcinoma with local venous invasion. METHODOLOGY: A systematic literature search (Medline, Embase, Cochrane Library, Biosis, Science Citation Index, Ovid Journals) was performed to identify all eligible articles from January 2000 to December 2009. The methodological quality of included studies on portal vein/superior mesenteric resection during pancreatectomy for pancreatic carcinoma was evaluated independently by 2 authors and 47 non-duplicated studies providing relevant data was found. Quantitative data on operation, perioperative results (blood loss, operative time, and length of hospital stay), mortality, morbidity, histopathology of resected specimens, adjuvant therapies, and overall outcome were extracted from included studies for systematic analysis. RESULTS: The median operating time was 480 (140-1340) min, blood loss 1420 (50-14280) ml and the length of hospital stay 16 (4-123) days. Operative mortality and postoperative morbidity rates ranged from 0 to 14.3 % and 6 % to 67 % with a median of 3.5 % and 33 %, respectively. Median survival was 15 months and ranged from 1.6 to 250 months, and 1-, 2-, 3- and 5-year survival rates ranged from 28.5 to 92, 6.7 to 81.1, 0 to 60.3 and 0 to 24 % with a media of 56.6, 31.5, 17 and 12 %, respectively. Specimen histopathology confirmed venous invasion, perineural invasion and lymphnodal involvement in 66.6,53 and 73%, respectively. CONCLUSIONS: In properly selected patients, pancreatectomy combined with portal vein/superior mesenteric resection is a feasible surgical procedure with a survival benefit for pancreatic carcinoma, and the systemic chemotherapy is indispensable as the common events of perineural invasion and lymphnodal involvement of the pancreatic carcinoma with local venous invasion.

Diagnostic and prognostic value of the methylation status of secreted frizzled-related protein 2 in colorectal cancer.

PURPOSE: The aim of this study was to investigate the diagnostic and prognostic significance of the methylation status of secreted frizzled-related protein 2 (SFRP2) in colorectal cancer (CRC). METHODS: Methylation-specific PCR assay was performed to analyze SFRP2 promoter methylation in solid tissue, stool and serum samples collected from 169 CRC patients, 63 patients with advanced adenomas, 46 patients with non-adenomatous polyps and 30 normal healthy controls. RESULTS: Methylated SFRP2 was frequently detected in CRC tissues and precancerous lesions. The sensitivity of SFRP2 methylation levels in tissue, fecal and serum DNA for the detection of CRC was similar, ranging from 66.9 to 88.2%; however, serum SFRP2 methylation levels showed a markedly higher specificity in discriminating CRCs from benign adenomas than those of SFRP2 methylation levels in tumor and fecal DNA. Moreover, serum SFRP2 methylation was significantly associated with poor differentiation grade (P=0.019), serosal/subserosal invasion (P < 0.001), lymph node metastasis status (P < 0.001) and TNM stage (P < 0.001) of CRC. CRC patients with SFRP2 hypermethylation in tumor, stool and serum samples had a significantly shorter overall survival than those negative for SFRP2 methylation (P=0.0216, 0.0219, and 0.0255, respectively). Multivariate Cox regression analysis revealed that SFRP2 promoter methylation in tumor samples was an independent prognostic factor for overall survival. CONCLUSION: Our data suggest that serum SFRP2 methylation status represents a promising, non-invasive marker for CRC detection and staging. Hypermethylated SFRP2 may have prognostic relevance in patients with CRC.

[Suspension with repose system in the treatment of obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To introduce the treatment of severe obstructive sleep apnea-hypopnea syndrome (OSAHS) with Repose bone screw system and to evaluate the treating effect. METHODS: Thirty-two patients with severe OSAHS (Friedman classification II, III) were treated with tongue ablation + uvulopalatopharyngoplasty + hard palate shortening + Repose suspension. All patients were followed-up for 6 months. Apnea hypopnea index (AHI), lowest oxygen percent saturation (LSaO2), body mass index (BMI), vallecula epiglottic-lateral pharyngeal wall (V-LPW) and pharyngeal airway space (PAS) were used for the diagnosis and evaluation. RESULTS: The AHI in 32 patients reduced from (78.3 +/- 11.6)/h to (18.4 +/- 12.5)/h (x(-) +/- s), t = 13.5, P = 0.000. The LSaO2 increased from (0.632 +/- 0.007) to (0.794 +/- 0.006), t = 4.1, P = 0.000. The BMI was statistical indiscriminate. The V-LPW increased from (12.1 +/- 3.2) mm to (16.9 +/- 2.6) mm (t = 2.5, P = 0.014). PAS increased from (9.2 +/- 3.3) mm to (15.6 +/- 2.4) mm (t = 7.6, P = 0.000). The total effective rate was 93.8%. Three genioglossus stabilization patients complained about foreign body sensation in the mouth floor 3 - 7 days after procedures, which disappeared in 6 months. One genioglossus stabilization patients complained about mandibular osteomyelitis 3 months after procedures, which recovered after anti-inflammatory treatment for 5 days. One genioglossus stabilization patients appeared hypoglossia bleeding, which stopped after compression. One hyoid suspension patients showed haematoma of submandibular region and cured after incision and drainage. CONCLUSION: Repose system was an effective method, safe, simple, with few complications.