BACKGROUND:During bone tissue healing,promoting the vascularization of new bone is a common strategy to accelerate the repair of bone tissue.However,the rapid fibrosis process during bone defect repair is often ignored.OBJECTIVE:To design and prepare a core-shell structure bionic scaffold to regulate the process of fibrosis and vascularization in new callus,characterize physical characteristics of the scaffold,and verify the anti-fibrosis and osteogenic properties in vitro and in vivo.METHODS:A core-shell structure bionic scaffold to regulate the process of fibrosis and vascularization in new callus was designed and prepared.The outer shell structure of the scaffold was composed of polycaprolactone electrospun nanofibers loaded with fibroblast activating protein inhibitor;and the inner core structure was composed of gelatin methacrylate hydrogel loaded with deferoxamine.The physical characteristics of electrospun and hydrogel were characterized,and the biocompatibility of the material was verified by live-dead staining and CCK-8 assay.The antifibrotic effect of core-shell structure was analyzed by fibroblast in vitro assay.The osteogenic effect of fibroblast activating protein inhibitor in core-shell structure was analyzed by MC3T3-E1 cells in vitro assay.The vasogenic effect of deferoxamine in core-shell structure was analyzed by human umbilical vein endothelial cells.The effect of bionic core-shell scaffold on bone repair was evaluated by critical bone defect test in rats.RESULTS AND CONCLUSION:(1)The core-shell structure bionic scaffold had good biocompatibility.Hydrophobic polycaprolactone electrospun fibers prepared by electrospinning technology could effectively block the ingrowth of exogenous fibrous tissue on the physical level.The electrospun fiber membrane could effectively release the anti-fibrosis drug fibroblast activating protein inhibitor within 2 weeks,and the released anti-fibrosis drug could inhibit the growth and adhesion of fibroblasts around bone defects,effectively reduced the expression of fibroblast-related proteins,promoted the expression of osteoblast protein in MC3T3-E1 cells,and accelerated its mineralization rate.The deferoxamine in the core-shell structure could promote the migration and vascular formation ability of human umbilical vein endothelial cells,and promoted their strong expression of"H"vascular characteristic protein.(2)In critical bone defect model of SD rats established in the femur,compared with polycaprolactone membrane,the core-shell structure bionic scaffold could effectively repair bone defects.(3)These findings indicate that the core-shell structure bionic scaffold can prevent excessive fibrosis of callus and promote the formation of"H"vessels in the new callus,which can effectively avoid the occurrence of nonunion and accelerate the repair process of critical bone defect.

BACKGROUND:Cell senescence is one of the major risk factors for osteoarthritis,but there is no widely accepted anti-osteoarthritis therapy targeting senescent cells.OBJECTIVE:To develop a feasible treatment strategy targeting senescent cells in osteoarthritis.METHODS:The cationic liposome containing rapamycin,RAPA@Lipo,was prepared by thin film dispersion method.Methylallylated hyaluronic acid hydrogel was synthesized,and RAPA@Lipo was added to the methylallylated hyaluronic acid hydrogel aqueous phase solution.The hydrogel microspheres were prepared by microfluidic equipment.Solid hydrogel microspheres(RAPA@Lipo@MS)were crosslinked under violet light.Primary human chondrocytes were co-cultured with RAPA@Lipo and RAPA@Lipo@MS,respectively.The biocompatibility of the materials was evaluated by CCK-8 assay and live/dead staining.Primary rat chondrocytes were cultured in four groups.Normal control group was cultured for 48 hours.The model group was stimulated with H2O2 for 24 hours to establish senescent cell model.RAPA@Lipo group and RAPA@Lipo@MS group were cultured for 24 hours after establishing senescent cell model with RAPA@Lipo and RAPA@Lipo@MS,respectively.After culture,immunofluorescence was used to observe the expression of p62 and type Ⅱ collagen.RT-PCR was used to detect the mRNA expression of interleukin 6,matrix metalloproteinase 13,type Ⅱ collagen,aggrecan,and ADAMTS-5.RESULTS AND CONCLUSION:(1)The results of CCK-8 assay and live/dead staining showed that RAPA@Lipo and RAPA@Lipo@MS had good biocompatibility.(2)Compared with the normal control group,the protein expression of p62 was increased(P<0.05);the expression of type Ⅱ collagen was decreased(P<0.05),and the mRNA expression levels of interleukin 6,matrix metalloproteinase 13,and ADAMTS-5 were increased(P<0.05);mRNA expression levels of type Ⅱ collagen and aggrecan were decreased(P<0.05)in the model group.Compared with the model group,the expression of p62 protein was decreased(P<0.05);the expression of type Ⅱ collagen was increased(P<0.05),and the mRNA expression levels of interleukin 6,matrix metalloproteinase 13,and ADAMTS-5 were decreased(P<0.05);mRNA expression of type Ⅱ collagen and aggrecan increased(P<0.05)in the RAPA@Lipo@MS group.(3)These findings indicate that RAPA@Lipo@MS can control the quality of cells in vivo by enhancing autophagy,reduce senescent cells in vivo,and locally eliminate senescent cells and senescence-associated secretory phenotype factors in osteoarthritis,thereby slowing the progression of osteoarthritis and creating a cartilage microenvironment that promotes regeneration.

Objective:Autoimmune gastritis (AIG) is characterized by the loss of acid-secreting glands, resulting in hypochlorhydria and hypergastrinemia, conditions that significantly increase the risk of developing gastric neuroendocrine tumors (NETs) and gastric adenocarcinoma. In recent years, AIG has garnered increasing attention in both clinical and research settings. However, comprehensive studies on the clinical and endoscopic characteristics of AIG particularly cases complicated by gastric neoplastic lesions remain limited in China. This study aims to comprehensively summarize the clinical and endoscopic features of AIG and its associated gastric neoplastic lesions.Methods:A retrospective analysis was conducted using medical records from patients with AIG diagnosed at Sichuan Provincial People′s Hospital between 2019 and 2024. Data collected included demographic information, medical history, serological test results, imaging findings, and endoscopic observations. The clinical and endoscopic features of AIG patients with gastric NETs or epithelial-derived tumors were compared to those without gastric neoplastic lesions to identify potential risk factors and diagnostic indicators for tumor development in AIG.Results:A total of 72 patients with AIG were included, of whom 62.5% (45/72) were female, with an age range of 30 to 79 years old (mean age: 57±11 years). Parietal cell antibody (PCA) positivity was observed in 93.1% (67/72), intrinsic factor antibody (IFA) positivity in 45.8% (33/72), and Helicobacter pylori ( H. pylori) co-infection in 48.6% (35/72). Endoscopically, 84.7% (61/72) showed prominent corpus-dominant advanced atrophy; 47.2% (34/72) had sticky adherent mucus; and 41.7% (30/72) displayed residual oxyntic mucosa in the gastric body or fundus. Only 23.6% (17/72) had normal antrum mucosa, and just 16.7% (12/72) showed a circular wrinkle-like pattern. Gastric neoplastic lesions were identified in 35 patients (48.6%), including 15 cases (20.8%) with NETs and 20 cases (27.8%) with epithelial-derived tumors (four adenocarcinomas, three adenomas, and 13 cases of intraepithelial neoplasia). No significant differences were found between tumor and non-tumor groups in terms of age, gender, PCA/IFA positivity, gastrin levels, anemia status, folic acid, or serum iron levels. However, patients with NETs had significantly lower vitamin B 12 levels compared to those without tumors (183±111 ng/L vs. 323±159 ng/L, t=2.47, P=0.042). Additionally, AIG patients with NETs were more likely to be H.pylori-negative compared to both the non-tumor group (66.7% vs. 35.1%, χ2=5.26, P=0.072) and the epithelial-derived tumor group (66.7% vs. 30.0%, χ2=5.80, P=0.055). The incidence of reverse atrophy in the epithelial-derived tumor group was significantly lower than that in the non-tumor group (65.0% vs. 91.9%, χ2=6.49, P=0.011) and the NETs group (65.0% vs. 93.3%, χ2=3.90, P=0.048).? Conclusion:In AIG patients with NETs, serum vitamin B 12 levels are significantly reduced, suggesting that vitamin B 12 deficiency may be a key risk factor or clinical indicator for NET development in AIG. Furthermore, NETs are more frequently observed in AIG patients without H.pylori infection, while epithelial-derived tumors are more commonly associated with H.pylori co-infection.

BACKGROUND:During bone tissue healing,promoting the vascularization of new bone is a common strategy to accelerate the repair of bone tissue.However,the rapid fibrosis process during bone defect repair is often ignored.OBJECTIVE:To design and prepare a core-shell structure bionic scaffold to regulate the process of fibrosis and vascularization in new callus,characterize physical characteristics of the scaffold,and verify the anti-fibrosis and osteogenic properties in vitro and in vivo.METHODS:A core-shell structure bionic scaffold to regulate the process of fibrosis and vascularization in new callus was designed and prepared.The outer shell structure of the scaffold was composed of polycaprolactone electrospun nanofibers loaded with fibroblast activating protein inhibitor;and the inner core structure was composed of gelatin methacrylate hydrogel loaded with deferoxamine.The physical characteristics of electrospun and hydrogel were characterized,and the biocompatibility of the material was verified by live-dead staining and CCK-8 assay.The antifibrotic effect of core-shell structure was analyzed by fibroblast in vitro assay.The osteogenic effect of fibroblast activating protein inhibitor in core-shell structure was analyzed by MC3T3-E1 cells in vitro assay.The vasogenic effect of deferoxamine in core-shell structure was analyzed by human umbilical vein endothelial cells.The effect of bionic core-shell scaffold on bone repair was evaluated by critical bone defect test in rats.RESULTS AND CONCLUSION:(1)The core-shell structure bionic scaffold had good biocompatibility.Hydrophobic polycaprolactone electrospun fibers prepared by electrospinning technology could effectively block the ingrowth of exogenous fibrous tissue on the physical level.The electrospun fiber membrane could effectively release the anti-fibrosis drug fibroblast activating protein inhibitor within 2 weeks,and the released anti-fibrosis drug could inhibit the growth and adhesion of fibroblasts around bone defects,effectively reduced the expression of fibroblast-related proteins,promoted the expression of osteoblast protein in MC3T3-E1 cells,and accelerated its mineralization rate.The deferoxamine in the core-shell structure could promote the migration and vascular formation ability of human umbilical vein endothelial cells,and promoted their strong expression of"H"vascular characteristic protein.(2)In critical bone defect model of SD rats established in the femur,compared with polycaprolactone membrane,the core-shell structure bionic scaffold could effectively repair bone defects.(3)These findings indicate that the core-shell structure bionic scaffold can prevent excessive fibrosis of callus and promote the formation of"H"vessels in the new callus,which can effectively avoid the occurrence of nonunion and accelerate the repair process of critical bone defect.

BACKGROUND:Cell senescence is one of the major risk factors for osteoarthritis,but there is no widely accepted anti-osteoarthritis therapy targeting senescent cells.OBJECTIVE:To develop a feasible treatment strategy targeting senescent cells in osteoarthritis.METHODS:The cationic liposome containing rapamycin,RAPA@Lipo,was prepared by thin film dispersion method.Methylallylated hyaluronic acid hydrogel was synthesized,and RAPA@Lipo was added to the methylallylated hyaluronic acid hydrogel aqueous phase solution.The hydrogel microspheres were prepared by microfluidic equipment.Solid hydrogel microspheres(RAPA@Lipo@MS)were crosslinked under violet light.Primary human chondrocytes were co-cultured with RAPA@Lipo and RAPA@Lipo@MS,respectively.The biocompatibility of the materials was evaluated by CCK-8 assay and live/dead staining.Primary rat chondrocytes were cultured in four groups.Normal control group was cultured for 48 hours.The model group was stimulated with H2O2 for 24 hours to establish senescent cell model.RAPA@Lipo group and RAPA@Lipo@MS group were cultured for 24 hours after establishing senescent cell model with RAPA@Lipo and RAPA@Lipo@MS,respectively.After culture,immunofluorescence was used to observe the expression of p62 and type Ⅱ collagen.RT-PCR was used to detect the mRNA expression of interleukin 6,matrix metalloproteinase 13,type Ⅱ collagen,aggrecan,and ADAMTS-5.RESULTS AND CONCLUSION:(1)The results of CCK-8 assay and live/dead staining showed that RAPA@Lipo and RAPA@Lipo@MS had good biocompatibility.(2)Compared with the normal control group,the protein expression of p62 was increased(P<0.05);the expression of type Ⅱ collagen was decreased(P<0.05),and the mRNA expression levels of interleukin 6,matrix metalloproteinase 13,and ADAMTS-5 were increased(P<0.05);mRNA expression levels of type Ⅱ collagen and aggrecan were decreased(P<0.05)in the model group.Compared with the model group,the expression of p62 protein was decreased(P<0.05);the expression of type Ⅱ collagen was increased(P<0.05),and the mRNA expression levels of interleukin 6,matrix metalloproteinase 13,and ADAMTS-5 were decreased(P<0.05);mRNA expression of type Ⅱ collagen and aggrecan increased(P<0.05)in the RAPA@Lipo@MS group.(3)These findings indicate that RAPA@Lipo@MS can control the quality of cells in vivo by enhancing autophagy,reduce senescent cells in vivo,and locally eliminate senescent cells and senescence-associated secretory phenotype factors in osteoarthritis,thereby slowing the progression of osteoarthritis and creating a cartilage microenvironment that promotes regeneration.

Objective:Autoimmune gastritis (AIG) is characterized by the loss of acid-secreting glands, resulting in hypochlorhydria and hypergastrinemia, conditions that significantly increase the risk of developing gastric neuroendocrine tumors (NETs) and gastric adenocarcinoma. In recent years, AIG has garnered increasing attention in both clinical and research settings. However, comprehensive studies on the clinical and endoscopic characteristics of AIG particularly cases complicated by gastric neoplastic lesions remain limited in China. This study aims to comprehensively summarize the clinical and endoscopic features of AIG and its associated gastric neoplastic lesions.Methods:A retrospective analysis was conducted using medical records from patients with AIG diagnosed at Sichuan Provincial People′s Hospital between 2019 and 2024. Data collected included demographic information, medical history, serological test results, imaging findings, and endoscopic observations. The clinical and endoscopic features of AIG patients with gastric NETs or epithelial-derived tumors were compared to those without gastric neoplastic lesions to identify potential risk factors and diagnostic indicators for tumor development in AIG.Results:A total of 72 patients with AIG were included, of whom 62.5% (45/72) were female, with an age range of 30 to 79 years old (mean age: 57±11 years). Parietal cell antibody (PCA) positivity was observed in 93.1% (67/72), intrinsic factor antibody (IFA) positivity in 45.8% (33/72), and Helicobacter pylori ( H. pylori) co-infection in 48.6% (35/72). Endoscopically, 84.7% (61/72) showed prominent corpus-dominant advanced atrophy; 47.2% (34/72) had sticky adherent mucus; and 41.7% (30/72) displayed residual oxyntic mucosa in the gastric body or fundus. Only 23.6% (17/72) had normal antrum mucosa, and just 16.7% (12/72) showed a circular wrinkle-like pattern. Gastric neoplastic lesions were identified in 35 patients (48.6%), including 15 cases (20.8%) with NETs and 20 cases (27.8%) with epithelial-derived tumors (four adenocarcinomas, three adenomas, and 13 cases of intraepithelial neoplasia). No significant differences were found between tumor and non-tumor groups in terms of age, gender, PCA/IFA positivity, gastrin levels, anemia status, folic acid, or serum iron levels. However, patients with NETs had significantly lower vitamin B 12 levels compared to those without tumors (183±111 ng/L vs. 323±159 ng/L, t=2.47, P=0.042). Additionally, AIG patients with NETs were more likely to be H.pylori-negative compared to both the non-tumor group (66.7% vs. 35.1%, χ2=5.26, P=0.072) and the epithelial-derived tumor group (66.7% vs. 30.0%, χ2=5.80, P=0.055). The incidence of reverse atrophy in the epithelial-derived tumor group was significantly lower than that in the non-tumor group (65.0% vs. 91.9%, χ2=6.49, P=0.011) and the NETs group (65.0% vs. 93.3%, χ2=3.90, P=0.048).? Conclusion:In AIG patients with NETs, serum vitamin B 12 levels are significantly reduced, suggesting that vitamin B 12 deficiency may be a key risk factor or clinical indicator for NET development in AIG. Furthermore, NETs are more frequently observed in AIG patients without H.pylori infection, while epithelial-derived tumors are more commonly associated with H.pylori co-infection.

OBJECTIVE: To present on a prenatally diagnosed case with complex structural rearrangements of chromosome 8. METHODS: Chromosome karyotyping, chromosomal microarray analysis (CMA) and fluorescence in situ hybridization (FISH) were carried out for a fetus with increased nuchal thickness. RESULTS: The karyotype of the amniotic fluid sample showed extra materials on 8p. FISH revealed a centromeric signal at the terminal of 8p with absence of telomeric signal. CMA revealed partial deletion of 8p23.3 [(208049_2256732)×1], partial duplication of 8p23.3p23.2 [(2259519_3016818)×3], and partial duplication of 8q [8q11.1q12.2(45951900_60989083)×3]. CONCLUSION The complex structural rearrangements of chromosome 8 in this case has differed from the commonly seen inv dup del(8p).
Female ; Pregnancy ; Humans ; Chromosomes, Human, Pair 8/genetics* ; In Situ Hybridization, Fluorescence ; Gene Rearrangement ; Prenatal Diagnosis ; Centromere

Objective:To investigate the effects of self-help mindfulness-based stress reduction (MBSR) training on illness uncertainty andsleep quality in patients with atrial fibrillation (AF) after radiofrequency ablation. To provide the basis for improving the quality of life of these patients.Methods:This was a randam controlled Test. A convenient sampling method was used to select 90 patients with atrial fibrillation who underwent radiofrequency ablation in the First Peoples Hospital of Changzhou from January 2021 to December 2021. According to the random number table method. They were divided into the experimental group and the control group, with 45 cases in each group. The control group received routine nursing, and the observation group received home-based self-help MBSR training based on the routine nursing. Five Facet Mindfulness Questionnaire (FFMQ), Mishel Uncertainty in Illness Scale and the Pittsburgh Sleep Quality Index Scale (PSQI) were used to evaluate the scores of each scale before intervention, 8 weeks and 3 months after intervention.Results:A total of 42 cases were completed in the experimental group and 41 cases in the control group. Repeated measurement analysis of variance showed that there were interaction effect ( F interaction = 90.98, 46.27, 39.61, all P<0.01), time effect ( F time = 298.67, 179.06, 76.32, all P<0.01) and inter-group effect ( F intergroup = 19.88, 4.07, 18.70, all P<0.05) on mindfulness score, disease uncertainty score, total score of sleep quality and scores of all dimensionsin between the two groups. Simple effect analysis showed that scores of all scales in experimental groups were significantly better than those in control group after the intervention ( F values were 11.75 to 66.49, all P<0.01). Conclusion:Self-help MBSR training can improve the level of mindfulness, reduce the feeling of uncertainty and improve the quality of sleep in patients with atrial fibrillation after radiofrequency ablation.

【Objective】 To evaluate the clinical efficacy and safety of one kind of human prothrombin complex concentrate in treatment of patients with hemophilia B. 【Methods】 The clinical data of 36 patients with hemophilia B treated with human prothrombin complex concentrate produced by Shenzhen Weiguang Biological Products Co. Ltd. from May 2018 to April 2019 were retrospectively analyzed, and its clinical efficacy and safety were analyzed. 【Results】 A total of 35 subjects entered the full analysis set (FAS)and safety set (SS), 33 subjects entered the per protocol Set (PPS). Thirty minutes after the first infusion of FAS subjects, the activity of coagulation factor Ⅸ increased from (3.93±0.975) IU/dL to (25.61±9.337) IU/dL, and the infusion efficiency was (96.43±22.007)%. The increased value of coagulation factor Ⅱ activity was (73.25±14.874) IU/dL. The activity of coagulation factor Ⅶ was (42.79±16.847) IU/dL. The increased value of coagulation factor Ⅹ activity was (65.29±17.042) IU/dL. The increased value of coagulation factor Ⅸ activity was (21.68±9.434%) IU/dL. Twenty-four hours after the first infusion of FAS subjects, the improvement of bleeding symptoms and signs was excellent in 21 cases (60%), improved in 14 cases (40.0%), and the effective rate was 100%. The incidence of adverse reactions was 2.9%(1/35), and there was no antibody to human coagulation factor Ⅸ and new virus infection. 【Conclusion】 Infusion of human prothrombin complex concentrate produced by Shenzhen Weiguang Biological Products Co. Ltd. in the treatment of hemophilia B has significant clinical efficacy and good safety.

OBJECTIVES: Nasopharyngeal carcinoma (NPC) is a highly invasive epithelial malignant tumor with unique geographical and ethnic distribution characteristics. NPC is mostly found in south China and Southeast Asia, and its treatment mainly depends on radiotherapy and chemotherapy. However, NPC is usually found in the late stage, and local recurrence and distant metastasis are common, leading to poor prognosis. The receptor tyrosine kinase AXL is up-regulated in various tumors and it is involved in tumor proliferation, migration, invasion, and other processes, which are associated with poor prognosis of tumors. This study aims to detect the expression of AXL in NPC cell lines and tissues, and to investigate its biological function of AXL and the underlying molecular mechanisms in regulation of NPC. METHODS: The expression levels of AXL in normal nasopharyngeal epithelial tissues and NPC tissues were analyzed by GSE68799, GSE12452, and GSE53819 data sets based on Gene Expression Omnibus (GEO) database. The Cancer Genome Atlas (TCGA) database was used to analyze the relationship between AXL and prognosis of head and neck squamous cell carcinoma (HNSC). The indicators of prognosis included overall survival (OS), disease-free interval (DFI), disease-specific survival (DSS), and progression-free interval (PFI). Western blotting assay was used to detect the AXL protein expression levels in normal nasopharyngeal epithelial cell line and NPC cell lines. Immunohistochemical method was used to detect AXL expression levels in normal nasopharyngeal epithelial tissues and NPC tissues. Cell lines with stable AXL knockdown were established by infecting 5-8F and Fadu cells with lentivirus interference vector, and cell lines with stable AXL overexpression were established by infecting C666-1 and HK-1 cells with lentivirus expression vector. Real-time PCR and Western blotting were used to detect the efficiency of knockdown and overexpression in stable cell lines. The effects of AXL knockdown or overexpression on proliferation, migration, and invasion of NPC cells were detected by CCK-8, plate colony formation, and Transwell assays, and the effect of AXL knockdown on tumor growth in nude mice was detected by subcutaneous tumor formation assay. The sequence of AXL upstream 2.0 kb promoter region was obtained by UCSC online database. The PROMO online database was used to predict AXL transcription factors with 0% fault tolerance, and the JASPAR online database was used to predict the binding sites of ETS1 to AXL. Real-time PCR and Western blotting were used to detect the effect of ETS1 on AXL protein and mRNA expression. The AXL upstream 2.0 kb promoter region was divided into 8 fragments, each of which was 250 bp in length. Primers were designed for 8 fragments. The binding of ETS1 to AXL promoter region was detected by chromatin immuno-precipitation (ChIP) assay to determine the direct regulatory relationship between ETS1 and AXL. Rescue assay was used to determine whether ETS1 affected the proliferation, migration, and invasion of NPC cells through AXL. RESULTS: Bioinformatics analysis showed that AXL was highly expressed in NPC tissues (P<0.05), and AXL expression was positively correlated with OS, DFI, DSS, and PFI in HNSC patients. Western blotting and immunohistochemical results showed that AXL was highly expressed in NPC cell lines and tissues compared with the normal nasopharyngeal epithelial cell line and tissues. Real-time PCR and Western blotting results showed that knockdown and overexpression efficiency in the stable cell lines met the requirements of subsequent experiments. The results of CCK-8, plate colony formation, Transwell assays and subcutaneous tumor formation in nude mice showed that down-regulation of AXL significantly inhibited the proliferation, migration, invasion of NPC cells and tumor growth (all P<0.05), and the up-regulation of AXL significantly promoted the proliferation, migration, and invasion of NPC cells (all P<0.05).As predicted by PROMO and JASPAR online databases, ETS1 was a transcription factor of AXL and had multiple binding sites in the AXL promoter region. Real-time PCR and Western blotting results showed that knockdown or overexpression of ETS1 down-regulated or up-regulated AXL protein and mRNA expression levels. ChIP assay result showed that ETS1 bound to AXL promoter region and directly regulate AXL expression. Rescue assay showed that AXL rescued the effects of ETS1 on proliferation, migration and invasion of NPC cells (P<0.05). CONCLUSIONS AXL is highly expressed in NPC cell lines and tissues, which can promote the malignant progression of NPC, and its expression is regulated by transcription factor ETS1.
Animals ; Cell Line, Tumor ; Cell Movement/genetics* ; Cell Proliferation/genetics* ; Gene Expression Regulation, Neoplastic ; Mice ; Mice, Nude ; Nasopharyngeal Carcinoma/genetics* ; Nasopharyngeal Neoplasms/metabolism* ; RNA, Messenger/genetics* ; Sincalide/metabolism* ; Transcription Factors/genetics*