Integrating network pharmacology and experimental validation reveals therapeutic effects of D-mannose on NAFLD through mTOR suppression.

Non-alcoholic fatty liver disease (NAFLD), a chronic liver condition and metabolic disorder, has emerged as a significant health issue worldwide. D-mannose, a natural monosaccharide widely existing in plants and animals, has demonstrated metabolic regulatory properties. However, the effect and mechanism by which D-mannose may counteract NAFLD have not been studied. In this study, network pharmacology followed by molecular docking analysis was utilized to identify potential targets of mannose against NAFLD, and the leptin receptor-deficient, genetically obese db/db mice was employed as an animal model of NAFLD to validate the regulation of D-mannose on core targets. As a result, 67 targets of mannose are predicted associated with NAFLD, which are surprisingly centered on the mechanistic target of rapamycin (mTOR). Further analyses suggest that mTOR signaling is functionally enriched in potential targets of mannose treating NAFLD, and that mannose putatively binds to mTOR as a core mechanism. Expectedly, repeated oral gavage of supraphysiological D-mannose ameliorates liver steatosis of db/db mice, which is based on suppression of hepatic mTOR signaling. Moreover, daily D-mannose administration reduced hepatic expression of lipogenic regulatory genes in counteracting NAFLD. Together, these findings reveal D-mannose as an effective and potential NAFLD therapeutic through mTOR suppression, which holds translational promise.

Characteristics and catalytic behavior of Ru-Sn bimetallic catalysts for TMCB hydrogenation to CBDO.

A series of Ru-Sn/γ-Al2O3 catalysts were prepared by the immersion method for tetramethylcyclobutane-1,3-dione (TMCB) hydrogenation to prepare 2,2,4,4-tetramethyl-1,3-cyclobutanediol (CBDO). The effect of the preparation method and reaction technology on TMCB hydrogenation activity was discussed. The catalysts were analyzed by means of XRD, BET, H2-TPR, XPS, scanning electron microscopy (SEM), and transmission electron microscopy (TEM), and it was found that the synthesized Ru was distributed on the surface of the carrier in the form of nanoparticles, showing a good catalytic effect. The results showed that when Ru loading was fixed at 5%, Sn was used as an auxiliary agent, and Ru/Sn = 1 : 1 as the catalyst, the reaction conditions were 120 °C, 4 MPa, and 1 h, and the catalytic hydrogenation effect of TMCB on CBDO was the best. The selectivity was as high as 73.5%, and the cis-trans ratio was 1.11. It may be the strong interaction between Ru and Sn under this ratio condition, which leads to the largest number of nano-active centers of elemental Ru. Finally, the reaction mechanism of TMCB hydrogenation to CBDO is discussed.

Tibial fracture surgery in elderly mice caused postoperative neurocognitive disorder via SOX2OT lncRNA in the hippocampus.

Increasing evidence indicates the major role of mitochondrial function in neurodegenerative disease. However, it is unclear whether mitochondrial dynamics directly affect postoperative neurocognitive disorder (PND). This study aimed to analyze the underlying mechanisms of mitochondrial dynamics in the pathogenesis of PND. Tibial fracture surgery was performed in elderly mice to generate a PND model in vivo. Cognitive behavior was evaluated 3 days post-surgery using novel object recognition and fear conditioning. A gradual increase in the SOX2OT mRNA level and decrease in the SOX2 mRNA level were noted, with impaired cognitive function, in the mice 3 days after tibial surgery compared with mice in the sham group. To evaluate the role of SOX2OT in PND, SOX2OT knockdown was performed in vitro and in vivo using lentivirus transfection in HT22 cells and via brain stereotactic injection of lentivirus, respectively. SOX2OT knockdown reduced apoptosis, inhibited oxidative stress, suppressed mitochondrial hyperdivision, attenuated surgery-induced cognitive dysfunction, and promoted downstream SOX2 expression in elderly mice. Furthermore, Sox2 alleviated mitochondrial functional damage by inhibiting the transcription of mitochondrial division protein Drp1. Our study findings indicate that SOX2OT knockout alleviates surgery-induced mitochondrial fission and cognitive function defects by upregulating the expression of Sox2 in mice, resulting in the inhibition of drp1 transcription. Therefore, regulation of the SOX2/Drp1 pathway may be a potential mechanism for the treatment of patients with PND.

Preparation, Characterization, and Performance of a Modified Polyacrylamide-Sericite Gel.

In this study, a modified chemical plugging agent is prepared with the aim to reduce the well moisture content and improve the efficiency of oilfield development. In comparison to other chemical plugging agents, the composite gels plugging agents have excellent blocking capacity and erosion resistance. In this study, optimal conditions for the preparation of plugging agents were explored. The results showed that the performance of polyacrylamide-sericite (PAM-sericite) gel improved at a polymerization temperature of 60 °C, a crosslinker concentration of 0.5%, an initiator concentration of 0.75%, an acrylamide concentration of 10.0%, and a sericite concentration of 10.0%. The characterization of PAM-sericite gel showed a certain fold-like shape with a smoother surface, indicating that the doped sericite makes the plugging agent more compact and firm. It was also found that the blocking ratio of the plugging agent can potentially reach 99.5% after the addition of sericite. Moreover, failure stress of the skeleton structure and the water swelling degree were increased by 63.5% and 51.2%, respectively. Additionally, long-term stability, temperature resistance, pressure resistance and pressure stability also showed improvement to varying degrees. It was concluded that this gel has better stability against different kinds of salt solutions and is not affected by particle size.

[Paeonol inhibits the phosphorylation of NF-κB p65 and the expression of inflammatory cytokines in mouse BV2 microglia induced by lipopolysaccharide].

Objective This study is aimed to investigate the effect of paeonol on inflammation of BV2 microglia induced by lipopolysaccharide (LPS), and the underlying mechanism. Methods Mouse BV2 microglia was cultured in vitro. BV2 microglia was pretreated with paeonol of different concentration for 24 hours, then stimulated by LPS for 12 hours. Cell viability was detected by CCK-8 assay. Morphological changes of microglia were monitored by microscopy. The mRNA expression of TNF-α, IL-1ß, IL-12 and IL-6 by BV2 microglia was measured by real time quantitative-PCR. The protein expression of NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) was determined by Western blot analysis. Results Paeonol treatment improved cell viability, and inhibited over-activation of BV2 microglia challenged by LPS. Paeonol treatment concentration-dependently suppressed LPS induced mRNA expression of inflammatory cytokines including TNF-α, IL-1ß, IL-6, and IL-12 by BV2 microglia. Phosphorylation of NF-κB p65, but not protein level of NF-κB p65, was suppressed by paeonol treatment in a concentration-dependent manner. Conclusion Paeonol inhibits LPS induced phosphorylation of NF-κB p65 and transcription of downstream proinflammatory cytokines in BV2 microglia.

Electrocatalytic Degradation of Levofloxacin, a Typical Antibiotic in Hospital Wastewater.

Presently, in the context of the novel coronavirus pneumonia epidemic, several antibiotics are overused in hospitals, causing heavy pressure on the hospital's wastewater treatment process. Therefore, developing stable, safe, and efficient hospital wastewater treatment equipment is crucial. Herein, a bench-scale electrooxidation equipment for hospital wastewater was used to evaluate the removal effect of the main antibiotic levofloxacin (LVX) in hospital wastewater using response surface methodology (RSM). During the degradation process, the influence of the following five factors on total organic carbon (TOC) removal was discussed and the best reaction condition was obtained: current density, initial pH, flow rate, chloride ion concentration, and reaction time of 39.6 A/m2, 6.5, 50 mL/min, 4‱, and 120 min, respectively. The TOC removal could reach 41% after a reaction time of 120 min, which was consistent with the result predicted by the response surface (40.48%). Moreover, the morphology and properties of the electrode were analyzed. The degradation pathway of LVX was analyzed using high-performance liquid chromatography-mass spectrometry (LC-MS). Subsequently, the bench-scale electrooxidation equipment was changed into onboard-scale electrooxidation equipment, and the onboard-scale equipment was promoted to several hospitals in Dalian.

Ethyl pyruvate ameliorate inflammatory response of sinonasal mucosa by inhibiting HMGB1 in rats with acute rhinosinusitis.

High mobility group box 1 (HMGB1) has been known to involve in the pathogenesis of many inflammatory diseases. The aim of this study was to establish animal model of acute rhinosinusitis (ARS), and determine whether ethyl pyruvate (EP) attenuate inflammatory response of sinonasal mucosa by inhibiting HMGB1 in ARS animals. Thirty-six Sprague Dawley (SD) rat were used as follows: six normal controls without intervention (group 1); thirty rats were used for establishment of ARS rats model by nasal insertion of Merocel sponge, and model rats without any treatments (group 2), treated with nasal drops of sterile saline (group 3), 10 µl EP (group 4), and 20 µl EP (group 5), twice a day for 5 days, respectively. Bacterial culture was done regularly and the main bacterial strains were identified using matrix-assisted laser desorption/ionization time of flight mass spectrometry. HMGB1 expression in sinonasal mucosa was detected by immunohistochemistry and RT-PCR. Serum levels of HMGB1, IL-6, and TNF-α were determined by ELISA. Data from 29 of 36 rats that had completed research were analyzed. Bacterial colony formation unit (CFU) of nasal secretion was significantly higher in each group of ARS rats compared with controls (p < 0.001). ARS rats treated with EP had only slightly decreased CFU, but significantly attenuated inflammatory response of sinonasal mucosa and decreased HMGB1 expression compared to those treated with saline alone (p < 0.001). Serum levels of HMGB1, IL-6 and TNF-α were significantly higher in ARS rats compared to controls, and decreased by EP treatments (p < 0.001). Nasal sponge packing led to acute inflammatory response of nasal sinus in rats, and increased the expression of HMGB1, IL-6, and TNF-α. Nasal drops with EP could attenuate the inflammation of sinonasal mucosa through inhibiting the expression of HMGB1, IL-6 and TNF-α in ARS rats.

Mir-142-3p Regulates Inflammatory Response by Contributing to Increased TNF-α in Chronic Rhinosinusitis With Nasal Polyposis.

OBJECTIVE: Previous studies suggested that microRNAs played an important role in the progression of inflammation and remodeling of chronic rhinosinusitis with nasal polyposis. However, the abnormal expression of microRNAs and regulation cytokine expression in nasal polyposis are not clear. METHOD: The miR-142-3p and tumor necrosis factor α (TNF-α) expression levels in chronic rhinosinusitis with nasal polyposis were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The miR-142-3p and TNF-α levels in human nasal epithelial cells (HNEpC) after stimulation by lipopolysaccharide (LPS) were detected by qRT-PCR. Moreover, HNEpCs were transfected by miR-142-3p mimics or inhibitor or cotransfected with si-TNF-α to evaluate the regulation of miR-142-3p on TNF-α which affects the production of inflammatory factors. RESULTS: The miR-142-3p and TNF-α were significantly higher in nasal mucosa of chronic rhinosinusitis with polyps patients compared to normal human. MiR-142-3p and TNF-α expression levels were increased after LPS stimulation in a dose- and time-dependent manner. Knockdown of miR-142-3p in HNEpCs downregulated TNF-α expression at both messenger RNA and protein levels. CONCLUSIONS: It is indicated that miR-142-3p may participate in the regulation of the body's inflammatory response through the LPS-TLR-TNF-α signaling pathway in chronic rhinosinusitis with nasal polyposis.

Preparation, Characteristics, and Application of Bifunctional TiO2 Sheets.

TiO2 is a high-reflectance material for preparing sheets during dry reagent chemical tests in detail. In this study, bifunctional TiO2 sheets with diffusive and reflective properties were prepared using TiO2 microspheres (particle size 2-3 µm) and cellulose acetate (CA). Factors such as the CA dosage, water content, mixing time, and the choice of surfactant were investigated. The structure and properties of the bifunctional TiO2 sheets were characterized by thermogravimetry and differential thermal analysis (TG-DAT), scanning electron microscopy (SEM), dynamic contact angle test and reflectance spectroscopy. By studying the above experimental results, it was concluded that the most optimal preparation conditions for preparing the bi-functional TiO2 sheets under natural drying conditions were as follows: the mass ratio of CA to TiO2 microspheres was 0.05:1; Triton-100 was used to improve the diffusion performance of the bifunctional sheets, after mixing for 5 h and coating. The light reflectivity of the bifunctional TiO2 sheets in the 420 to 800 nm range was higher than 90%. Serum diffused in the bifunctional TiO2 sheets reacted in the reagent sheets and formed uniform colorful spots. Considering the repeatability of spot proportion and light reflectivity, the sheet offered a uniform serum diffusion and good repeatability. So, the bifunctional TiO2 sheets are nominated as a promising material for dry chemical diagnostic reagents.

Identification of a Novel MYO15A Mutation in a Chinese Family with Autosomal Recessive Nonsyndromic Hearing Loss.

Autosomal recessive nonsyndromic hearing loss (ARNSHL) is a genetically heterogeneous sensorineural disorder, generally manifested with prelingual hearing loss and absence of other clinical manifestations. The aim of this study is to identify the pathogenic gene in a four-generation consanguineous Chinese family with ARNSHL. A novel homozygous variant, c.9316dupC (p.H3106Pfs*2), in the myoxin XVa gene (MYO15A) was identified by exome sequencing and Sanger sequencing. The homozygous MYO15A c.9316dupC variant co-segregated with the phenotypes in the ARNSHL family and was absent in two hundred normal controls. The variant was predicted to interfere with the formation of the Myosin XVa-whirlin-Eps8 complex at the tip of stereocilia, which is indispensable for stereocilia elongation. Our data suggest that the homozygous MYO15A c.9316dupC variant might be the pathogenic mutation, and exome sequencing is a powerful molecular diagnostic strategy for ARNSHL, an extremely heterogeneous disorder. Our findings extend the mutation spectrum of the MYO15A gene and have important implications for genetic counseling for the family.

Efficacy of the modified endoscopic frontal sinus surgery for recurrent chronic frontal sinusitis.

To modify the endoscopic frontal sinus surgery and improve the therapeutic effect of recurrent chronic frontal sinusitis (RCFS). Eighty-five patients with RCFS were divided into two groups. Endoscopic frontal sinus surgery through an approach of Frontomaxillary Process-Agger Nasi, a modified Draf IIb procedure, was carried out in 51 patients (Group A), and conservative medication was applied in 34 patients as control (Group B). The therapeutic effect was prospectively evaluated with statistically validated measures of sinusitis-specific quality of life, sino-nasal outcome test-20 questionnaire (SNOT-20). Compared with pre-treatment, the average total score of SNOT-20 in RCFS patients was significantly decreased at the time of 6, 12 months after modified endoscopic frontal sinus surgery and medical treatments (p < 0.05). However, the total score of SNOT20 was significantly lower in group A than group B at the same period of the follow-up after treatments (p < 0.05). The overall efficacy evaluated by patients' self showed that the rate of "much improved" and "improved" was respectively 68.6 and 17.6 % in group A, and significantly better than group B (p < 0.001). Furthermore, the frontal sinus patency rate in group A was 85 %, and significantly higher than group B (p < 0.001). Endoscopic frontal sinus surgery through an approach of Frontomaxillary Process-Agger Nasi, a modified Draf IIb procedure, is an effective procedure to treat the RCFS.

WIP1 regulates the proliferation and invasion of nasopharyngeal carcinoma in vitro.

Wild-type p53-induced phosphatase (WIP1) is overexpressed and functionally altered in multiple human malignancies. The present study investigated its abnormal expression and dysfunctions in nasopharyngeal carcinoma (NPC) in vitro. Here, analysis of WIP1 mRNA and protein in human NPC tissues revealed that both WIP1 messenger RNA (mRNA) and protein were elevated and were correlated with NPC clinical stage and metastasis in patients. In vitro experiments further showed that WIP1 inhibition led to a decrease in the proliferative ability of NPC CNE-2 and 5-8F cells accompanied by cell cycle arrest and increased apoptosis. In addition, WIP1 knockdown inhibited the invasiveness of CNE-2 and 5-8F cells and was associated with the down-regulation of the expression of matrix metallopeptidase 9 (MMP-9) mRNA and protein. Taken together, our data demonstrate that WIP1 regulates the proliferation and invasiveness of NPC cells in vitro, and this may be correlated with its modulation of MMP-9 expression, cell cycle progression and apoptosis. WIP1 functioned as a potential therapeutic target in NPC management.

Genomic methylation profiling combined with gene expression microarray reveals the aberrant methylation mechanism involved in nasopharyngeal carcinoma taxol resistance.

Taxol is a first-line chemoagent used for treatment of nasopharyngeal carcinoma (NPC). A major obstacle to achieving successful treatment is the development of cellular taxol drug resistance. Aberrant DNA methylation has been recognized to be associated with the transcriptional inactivation of genes related to cancer drug resistance development. To identify the mechanism of DNA methylation involved in NPC taxol resistance, we applied a genome-wide DNA methylation microarray assay to reveal methylation alteration in taxol-resistant NPC cell lines (CNE-1/taxol, 5-8F/taxol, HNE-2/taxol) established previously in our laboratory. Combining with gene expression microarray, we identified drug resistance-associated genes in taxol-resistant cell lines. We also investigated the coeffect of taxol and the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) to confirm the involvement of DNA methylation. The methylation profiling revealed differential patterns between the drug-sensitive and -resistant cell lines. As a result, taxol-resistant cell lines were detected to be globally hypermethylated. Forty-eight differentially methylated genes (30 hypermethylated and 18 hypomethylated) were further identified commonly in the three taxol-resistant cell lines. Six of them (DLC1, CHFR, ABCC5, PEG10, ERBB2, and GSTP1) were independently confirmed to contribute to taxol resistance by both methylation-specific PCR and quantitative real-time PCR. Finally, we conclude that DNA methylation is closely correlated with taxol drug resistance in NPC cells. Combined analysis of DNA methylation and gene expression may enable the discovery of new therapeutic targets and prognostic biomarkers of cancers. Furthermore, DNA methylation inhibitors can reverse chemoresistance and prevent the development of acquired drug resistance.

[The aspergillus laryngotracheobronchitis. A case report and literature review].

The patient presented with dry cough, lending, fever and progressive dyspnea for two weeks. The patient had a prior respiratory infection history and the symptoms were not obvious, Early X-ray showed lung infection. Under the fibrolaryngoscope, the lingual surfaces of the epiglottis, epiglottic vallecula, and bilateral vocal cords were covered by yellow pseudomembrane. The motion of vocal cords was normal with poor glottic closure, and no ulcer was noted. Endotracheal mucosa was swelling and congested with an uneven surface, and purulent discharge and pseudomembrane was formed. Pathological examination revealed Aspergillus. The disease was diagnosed as Aspergillus laryngotracheobronchitis.

Inhibition of α folate receptor resulting in a reversal of taxol resistance in nasopharyngeal carcinoma.

OBJECTIVE: To further determine the role of FOLR1 in taxol resistance of nasopharyngeal carcinoma (NPC) and whether inhibition of FOLR1 expression reverses the taxol-resistant phenotype. STUDY DESIGN: Correlation study between gene expression and cancer cell survival. SETTING: University hospital. SUBJECTS AND METHODS: Three taxol-resistant sub-cell lines with a different resistant index were established from the parental CNE-1 NPC cell line. The correlation between FOLR1 expression and taxol sensitivity was statistically analyzed. Inhibition of FOLR1 expression was carried out by RNA interference and by a FOLR1-specific monoclonal antibody, and taxol sensitivity was examined by colony formation assays. FOLR1 expression was also examined in 72 NPC patient specimens by immunohistochemistry. RESULTS: The levels of FOLR1 expression were positively and significantly correlated with a taxol resistance phenotype (P < .05). Inhibition of FOLR1 expression resulted in a significantly increased sensitivity of taxol to taxol-resistant NPC cells (P < .05). An increase of FOLR1 expression by gene transfection caused a taxol-resistant phenotype in parental NPC cells. The level of FOLR1 expression was found to be related to clinical stage in NPC tissue samples. CONCLUSION: These results suggest that FOLR1 plays an important role in taxol resistance of NPC cells.

[Expression of human beta-defensin after endoscopic sinus surgery for chronic sinusitis].

OBJECTIVE: To observe the expressions of human beta-defensin 1 and 2 (hBD-1 and hBD-2) in nasal mucosa before and after the endoscopic sinus surgery and investigate the effects of hBD-1 and hBD-2 on the healing process after the surgery. METHODS: The patients undergoing endoscopic sinus surgery for chronic sinusitis were divided into 3 groups according to the response to the surgery, namely cured group, response group and non-response group. With those from healthy control subjects as the control, nasal mucosa samples were collected from the patients at 1 week, 2 weeks, 1 month, 3 months and 6 months after the surgery for detection of hBD-1 and hBD-2 mRNA and protein expressions by RT-PCR and Western blotting. RESULTS: hBD-1 and hBD-2 were expressed in both normal and chronic sinusitis mucosa, but the expression levels varied significantly between the individuals. The expression levels of hBD-2 was significantly correlated to the patients' response to the surgical treatment (P<0.05). hBD-1 showed slight differences between the individuals, but was not associated with the patients' prognosis. CONCLUSION: The expressions of hBD-2 mRNA and protein are significantly increased in patients with good response to endoscopic sinus surgery for chronic sinusitis, suggesting the value of hBD-2 as an indicator of the patients' prognosis.

[Role of folate receptor 1 in paclitaxel-resistance of nasopharyngeal carcinoma cells].

OBJECTIVE: To provide experimental evidence for the folate receptor 1 (FOLR1) mediated targeted cancer therapy and resistance reversal, the FOLR1 expression differences in nasopharyngeal carcinoma cells (CNE-1) and immortalized normal nasopharyngeal cells (NP69) and the correlation between FOLR1 expression and paclitaxel resistance index in nasopharyngeal carcinoma were investigated. METHODS: The expressions of FOLR1 in CNE-1, CNE-1/Taxol (paclitaxel-resistance cells) and NP69 was detected by cDNA microarray, reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot and immunocytochemistry. Proliferation inhibition rates of CNE-1 and CNE-1/Taxol cells were measured by colony formation assay after treated by short interfering RNA (siRNA) of FOLR1. RESULTS: The expressions of FOLR1 gene in CNE-1/Taxol cells and CNE-1 cells were 2636.0 and 176.0, respectively. The expression of FOLR1 was not detected in the NP69 by semi-quantative RT-PCR and Western blot. The high expression of FOLR1 in CNE-1/Taxol was verified by semi-quantative RT-PCR, and its expression level was positively correlated to the degree of drug-resistance (r(2) = 0.8719). The results were also validated by Western blot and immunocytochemistry. The sensitivity of CNE-1/Taxol to paclitaxel significantly increased after inhibition of FOLR1 gene expression by siRNA, and its IC(50) value was decreased by 59.6% (t = 6.92, P < 0.01). CONCLUSIONS: The expression of FOLR1 is closely related to the occurrence of NPC and Taxol resistance. FOLR1 gene may be one of the important target molecules in NPC treatment and reversion of the paclitaxel-resistance in NPC.

[Monostotic fibrous dysplasia of the sphenoid sinus: two cases report and literature review].

OBJECTIVE: To study the etiopathogenesis, clinical features, diagnosis and treatments of monostotic fibrous dysplasia of the sphenoid sinus. METHOD: Two cases of monostotic fibrous dysplasia of the sphenoid sinus without any symptoms was reported with relevant literature review. RESULT: No aggravation was found after 6 months-follow-up. CONCLUSION: The cranial fibrous dysplasia has low incidence rate with non-specific symptoms and high rate of misdiagnosis. The monostotic fibrous dysplasia of the sphenoid sinus without any symptom is rarely seen clinically. Imagiological examination, for example, CT and MRI, is valuable for the diagnosis of this disease. The histopathological evidence is absolutely necessary to make definite diagnosis. The conservative treatment may be chosen for the asymptomatic cases. Nasal Endoscopic surgery can not only remove the diseased region but also make diagnosis. The long-term follow-up should be carried out in all of these patients.

[Expression and significance of human beta-defensin in recurrent nasal polyps].

OBJECTIVE: To observe the expression of human beta-defensin-1 (hBD-1) and human beta-defensin-2 (hBD-2) in recurrent nasal polyps, and to investigate the role of beta-defensin in the recurrent nasal polyps. METHODS: Tissues of nasal polyps was obtained from 10 patients with nasal polyps undergoing endoscopic sinus surgery, recurrent nasal polyps from 10 patients 6 months after surgery, nasal mucosa from 10 recovered patients with nasal polyps postoperatively and,10 control subjects. hBD-1 mRNA and hBD-2 mRNA levels of tissue specimens in all groups were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: There was no significant difference in hBD-1 mRNA level between the 4 groups (P>0.05). Expression of hBD-2 mRNA was detected in patients with nasal polyps and recurrent nasal polyps, but rare in the recovered patients and the control subjects. CONCLUSION: hBD-1 is a constitutive expression and hBD-2 is an induced expression. beta-Defensin may play an important role in forming the nasal polyps.