Effective Use of Sugarcane-Bagasse-Derived KOH-Activated Biochar for Remediating Norfloxacin-Contaminated Water.

Bagasse-derived biochar (SCB750) was prepared at 750 °C using Chinese sugarcane bagasse as a carbon source and then modified with KOH for the removal of the antibiotic norfloxacin (NOR) from aqueous solutions. 3K-SCB750, prepared using a solid-to-liquid mass ratio of bagasse:KOH = 1:3, was found to have the best adsorption performance for NOR. Under the conditions of pH 5, 25 °C, 2.4 g L-1 adsorbent, and 300 mg L-1 NOR, its adsorption of NOR reached equilibrium (97.5% removal) after 60 min. The adsorption behaviours were in line with the quasi-second-order kinetic and Langmuir isotherm models, respectively. The maximum theoretical adsorption capacity reached up to 157.4 mg·g-1 at 40 °C. The thermodynamic parameters showed that the adsorption of NOR onto 3K-SCB750 was a spontaneous, endothermic, and physical process. In addition, Brunauer-Emmett-Teller analysis (BET), scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), and Raman spectroscopy were conducted to investigate the structural and adsorption properties of 3K-SCB750. Fourier transform infrared spectroscopy (FTIR) was also applied to understand the mechanism of adsorption of NOR onto 3K-SCB750. All of the results indicated that 3K-SCB750 had a large specific surface area of 1038.8 m2·g-1, an average pore size of 1.9 nm, and hierarchical structures with random pores and cracks for efficient removal of NOR. NOR adsorption mechanisms on 3K-SCB750 were related to the pore-filling effect and electrostatic attraction. Therefore, 3K-SCB750 biochar may be used as a promising adsorbent of antibiotics in wastewaters.

Histone deacetylase inhibitors promote epithelial-mesenchymal transition in Hepatocellular Carcinoma via AMPK-FOXO1-ULK1 signaling axis-mediated autophagy.

Hepatocellular carcinoma (HCC) is the third most frequent cause of cancer-related deaths globally because of high metastasis and recurrence rates. Elucidating the molecular mechanisms of HCC recurrence and metastasis and developing effective targeted therapies are expected to improve patient survival. The promising anti-cancer agents for the treatment of hematological malignancies, histone deacetylase inhibitors (HDIs), have limited effects against epithelial cell-derived cancers, including HCC, the mechanisms involved have not been elucidated. Herein, we studied the molecular mechanisms underlying HDI-induced epithelial-mesenchymal transition (EMT) involving FOXO1-mediated autophagy. Methods: The biological functions of HDIs in combination with autophagy inhibitors were examined both in vitro and in vivo. Cell autophagy was assessed using the generation of mRFP-GFP-LC3-expressing cells and fluorescent LC3 puncta analysis, Western blotting, and electron microscopy. An orthotopic hepatoma model was established in mice for the in vivo experiments. Results: Our study provided novel mechanistic insights into HDI-induced EMT mediated by the autophagy AMPK-FOXO1-ULK1-Snail signaling axis. We demonstrated that autophagy served as a pro-metastasis mechanism in HDI-treated hepatoma cells. HDIs induced autophagy via a FOXO1-dependent pathway, and FOXO1 inhibition promoted HDI-mediated apoptosis in hepatoma cells. Thus, our findings provided novel insights into the molecular mechanisms underlying HDI-induced EMT involving FOXO1-mediated autophagy and demonstrated that a FOXO1 inhibitor exerted a synergistic effect with an HDI to inhibit cell growth and metastasis in vitro and in vivo. Conclusion: We demonstrated that HDIs triggers FOXO1-dependent autophagy, which ultimately promotes EMT, limiting the clinical outcome of HDI-based therapies. Our study suggests that the combination of an HDI and a FOXO1 inhibitor is an effective therapeutic strategy for the treatment of HCC.

Histone deacetylase inhibitors upregulate Snail via Smad2/3 phosphorylation and stabilization of Snail to promote metastasis of hepatoma cells.

Hepatocellular carcinoma (HCC) remains the third most common cause of cancer-related mortality. Resection and transplantation are the only curative treatments available, but are greatly hampered by high recurrence rates. Histone deacetylase inhibitors (HDACIs) are considered to be promising anticancer agents in drug development. Currently, four HDACIs have been granted Food and Drug Administration (FDA) approval for cancer. HDACIs have shown significant efficacy in hematological malignancies. However, they have limited effects in epithelial cell-derived cancers, including HCC, and the mechanisms of these are not elucidated. In this study, our results demonstrated that HDACIs were able to induce epithelial-mesenchymal transitions (EMT) in hepatoma cells which are believed to trigger tumor cell invasion and metastasis. We found that HDACIs promoted the expression of Snail and Snail-induced EMT was critical for HDACI-initiated invasion and metastasis. We indicated that HDACIs upregulated Snail in two ways. Firstly, HDACIs upregulated Snail at the transcriptional level by promoting Smad2/3 phosphorylation and nuclear translocation, then combined with the promoter to activate the transcription of Snail. Secondly, we showed that HDACIs regulated the stabilization of Snail via upregulating the expression of COP9 signalosome 2 (CSN2), which combined with Snail and exposed its acetylation site, then promoted acetylation of Snail, thereby inhibiting its phosphorylation and ubiquitination to repress the degradation of Snail. All these results highlighted that HDACIs have limited effects in HCC, and the use of HDACIs combined with other targeted strategies to inhibit EMT, which explored in this study is a promising treatment method for treating HCC.

microRNA-889 is downregulated by histone deacetylase inhibitors and confers resistance to natural killer cytotoxicity in hepatocellular carcinoma cells.

Major histocompatibility complex class I chain-related gene B (MICB) is expressed on tumor cells and participates in natural killer (NK) cell-mediated antitumor immune response through engagement with the NKG2D receptor. This study was undertaken to identify novel microRNA (miRNA) regulators of MICB and clarify their functions in NK cell-mediated cytotoxicity to hepatocellular carcinoma (HCC) cells. Bioinformatic analysis and luciferase reporter assay were conducted to search for MICB-targeting miRNAs. Overexpression and knockdown experiments were performed to determine the roles of candidate miRNAs in the susceptibility of HCC cells to NK lysis. miR-889 was identified as a novel MICB-targeting miRNA and overexpression of miR-889 significantly inhibited the mRNA and protein expression of MICB in HepG2 and SMMC7721 HCC cells. miR-889 expression had a negative correlation with MICB mRNA levels in HCC specimens (r = -0.392, P = 0.0146). NK cell-mediated cytotoxicity was reduced in miR-889-overexpressing HCC cells, which was reversed by restoration of MICB expression. In contrast, knockdown of miR-889 led to more pronounced NK cell-mediated lysis in HCC cells. HCC cells exposed to the histone deacetylase (HDAC) inhibitor sodium valproate showed downregulation of miR-889. Enforced expression of miR-889 prevented the upregulation of MICB and enhancement of NK cell-mediated lysis by HDAC inhibitors. In conclusion, miR-889 upregulation attenuates the susceptibility of HCC cells to NK lysis and represents a potential target for improving NK cell-based antitumor therapies.

Curcumin downregulates the expression of Snail via suppressing Smad2 pathway to inhibit TGF-ß1-induced epithelial-mesenchymal transitions in hepatoma cells.

Hepatocellular carcinoma (HCC) remains the third cause of cancer-related mortality. Resection and transplantation are the only curative treatments available but are greatly hampered by high recurrence rates and development of metastasis, the initiation of cancer metastasis requires migration and invasion of cells, which is enabled by epithelial-mesenchymal transitions (EMT). TGF-ß1 is a secreted protein that performs many cellular functions, including the control of cell growth, cell proliferation, cell differentiation and apoptosis. TGF-ß1 is known as a major inducer of EMT, and it was reported that TGF-ß1 induced EMT via Smad-dependent and Smad-independent pathways. However, the extrinsic signals of TGF-ß1 regulated the EMT in hepatoma cells remains to be elucidated, and searching drugs to inhibit TGF-ß1 induced EMT may be considered to be a potentially effective therapeutic strategy in HCC. Fortunately, in this study, we found that curcumin inhibited TGF-ß1-induced EMT in hepatoma cells. Furthermore, we demonstrated that curcumin inhibited TGF-ß1-induced EMT via inhibiting Smad2 phosphorylation and nuclear translocation, then suppressing Smad2 combined with the promoter of Snail which inhibited the transcriptional expression of Snail. These findings suggesting curcumin could be a useful agent for antitumor therapy and also a promising drug combined with other strategies to preventing and treating HCC.

Bortezomib Relieves Immune Tolerance in Nasopharyngeal Carcinoma via STAT1 Suppression and Indoleamine 2,3-Dioxygenase Downregulation.

Radiotherapy is the primary treatment for nasopharyngeal carcinoma (NPC). Patients with intermediate and advanced stage NPC receiving only radiotherapy have limited survival, so newer immunotherapeutic approaches are sought. The major impediment to better clinical outcomes is tumor immune tolerance. Indoleamine 2,3-dioxygenase (IDO), an IFNγ-inducible enzyme, is a major inducer of immune tolerance during tumor development; therefore, inhibition of the IDO pathway is an important modality for cancer treatment. We show that bortezomib, a proteasomal inhibitor, inhibited the pathways leading to STAT1 and IRF-1 activation, both of which are necessary for IDO expression. Bortezomib downregulated IFNγ-induced IDO expression via inhibition of STAT1 phosphorylation and nuclear translocation, thereby suppressing STAT1-driven IDO transcription in NPC cells. Bortezomib also promoted IκB-α phosphorylation-ubiquitination, which released NF-κB from IκB-α. However, the released NF-κB could not enter the nucleus to conduct its biological effects and accumulated in the cytoplasm. Negative feedback inhibited the transcription of NF-κB, which is important for activating IRF-1 expression. IDO expression is regulated by two important transcription factor binding sites, ISREs, which bind STAT1 and IRF-1, and GASs, which binds STAT1. Bortezomib upregulated IRF-1 protein by inhibiting its proteasome-dependent degradation, but it also inhibited STAT1 phosphorylation, which directly inhibited the activation of GAS and indirectly inhibited the activation of ISRE, which needs both STAT1 and IRF-1. These discoveries provide a mechanism for the antitumor action of bortezomib and have implications for the development of clinical cancer immunotherapy for preventing and treating NPC. Cancer Immunol Res; 5(1); 42-51. ©2016 AACR.

The management of patients with esophageal cancer and coronary artery stenosis undergoing radiotherapy or concurrent chemoradiotherapy: a single-center experience.

PURPOSE: The incidence of esophageal cancer (EC) patients with coronary artery stenosis presents particular challenges. The aim of this retrospective study was to evaluate the efficiency of management on patients with both diseases treated by radiotherapy (RT) or concurrent chemoradiotherapy (CCRT). METHODS: Fifty-three patients with both EC and coronary artery stenosis from June 2009 to August 2012 were retrospectively analyzed. The patients received RT or CCRT with coronary artery stenosis management. Cardiac treatments often prescribed included aspirin, ß-blockers, statins etc. The adverse effects, overall response rate (ORR), progression-free survival (PFS) and overall survival (OS) were analyzed. RESULTS: Most of the patients were 40-70 years old. There were 25 patients in the CCRT group and 28 patients in the RT group. The complete response (CR) rate was higher in the patients in the CCRT group than in those in the RT group (48.0 vs 21.4%; p=0.041). The median PFS was 15.9 months in the CCRT group and 11.6 months in the RT group (p=0.025). OS was 22.4 months in the CCRT group and 15.8 months in the RT group (p=0.013). Though adverse effects were less in the RT group, no significance differences in grade 3-4 toxicity were observed. CONCLUSION: With the appropriate of coronary artery stenosis management, RT and CCRT were both tolerable and effective in EC patients with coronary artery stenosis.

Laparoscopic versus open hepatectomy for hepatocellular carcinoma: long-term outcomes.

PURPOSE: This study compared the longterm survival outcomes of patients with hepatocellular carcinoma (HCC) who underwent laparoscopic hepatectomy with those who were subjected to open hepatectomy. METHODS: This was a retrospective, case-control study; patients in the 2 groups were matched according to age, sex, body mass index (BMI), liver function, underlying liver disease, American Society of Anesthesiologists (ASA) score, tumor location and type of resection. A total of 118 patients (laparoscopy, N = 59; open, N = 59) were assessed. RESULTS: Patient characteristics did not differ between the groups. Postoperative 30-day complication rates did not differ between the groups. Pathological data did not differ between the two groups. The 5-year overall survival (OS) and disease-free survival (DFS) were not different between the laparoscopy and open groups. The laparoscopic approach was not an independent risk factor for tumor recurrence or mortality compared with the open approach. CONCLUSION: We found no differences in the oncologic outcomes between laparoscopic and open hepatectomy groups, suggesting that laparoscopic hepatectomy for HCC is a safe and effective option that does not increase the risk of serious complications.

The application of the fibroblast activation protein α-targeted immunotherapy strategy.

Cancer immunotherapy has primarily been focused on attacking tumor cells. However, given the close interaction between tumor cells and cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME), CAF-targeted strategies could also contribute to an integrated cancer immunotherapy. Fibroblast activation protein α (FAP α) is not detectible in normal tissues, but is overexpressed by CAFs and is the predominant component of the stroma in most types of cancer. FAP α has both dipeptidyl peptidase and endopeptidase activities, cleaving substrates at a post-proline bond. When all FAP α-expressing cells (stromal and cancerous) are destroyed, tumors rapidly die. Furthermore, a FAP α antibody, FAP α vaccine, and modified vaccine all inhibit tumor growth and prolong survival in mouse models, suggesting FAP α is an adaptive tumor-associated antigen. This review highlights the role of FAP α in tumor development, explores the relationship between FAP α and immune suppression in the TME, and discusses FAP α as a potential immunotherapeutic target.

Curcumin combined with FAPαc vaccine elicits effective antitumor response by targeting indolamine-2,3-dioxygenase and inhibiting EMT induced by TNF-α in melanoma.

Fibroblast activation protein α (FAPα) is a potential target for cancer therapy. However, elimination of FAPα+ fibroblasts activates secretion of IFN-γ and TNF-α. IFN-γ can in turn induce expression indolamine-2,3-dioxygenase (IDO), thereby contributing to immunosuppression, while TNF-α can induce EMT. These two reactive effects would limit the efficacy of a tumor vaccine. We found that curcumin can inhibit IDO expression and TNF-α-induced EMT. Moreover, FAPαc vaccine and CpG combined with curcumin lavage inhibited tumor growth and prolonged the survival of mice implanted with melanoma cells. The combination of FAPαc vaccine, CpG and curcumin stimulated FAPα antibody production and CD8+ T cell-mediated killing of FAPα-expressing stromal cells without adverse reactive effects. We suggest a combination of curcumin and FAPαc vaccine for melanoma therapy.

[Sodium butyrate down-regulates IFN-γ-induced indoleamine 2, 3 dioxygenase and promotes its acetylation and ubiquitination in CNE2 nasopharyngeal carcinoma cells].

OBJECTIVE: To investigate molecular mechanisms of posttranslational regulation of sodium butyrate (NaB) on indoleamine 2, 3-dioxygenase (IDO) expression induced by interferon γ (IFN-γ) in CNE2 nasopharyngeal carcinoma cells. METHODS: Western blotting and co-immunoprecipitation assay were used to detect the expression, acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells. RESULTS: Western blotting demonstrated that while the cells were treated with IFN-γ and NaB compared with IFN-γ treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-γ and NaB compared with the ones treated with IFN-γ only, acetylation and ubiquitination of IDO increased significantly. Western blotting showed that the cells treated with NaB and IFN-γ presented with lower IDO protein expression than the ones treated with NaB, IFN-γ and bortezomib simultaneously. CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-γ in a dose-dependent manner, and the combined treatment of IFN-γ and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.

Recombinant Cpn 0810 stimulates proinflammatory cytokine expression and apoptosis in human monocytes.

The aim of the present study was to express the recombinant Chlamydophila pneumoniae (C. pneumoniae) protein, Cpn 0810, in Escherichia coli (E. coli) BL21, and investigate the effects of Cpn 0810 on inflammatory and apoptotic processes in human monocytic (THP-1) cells. An ELISA was performed to detect the levels of the proinflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-6. In addition, Hoechst 33258 staining and annexin V binding analyses were performed to measure the rates of apoptosis. Purified glutathione S-transferase (GST)-Cpn 0810 recombinant proteins were obtained from the E. coli BL21 cells carrying the pGEX6p-2/Cpn 0810 plasmid, and were shown to stimulate the expression of TNF-α and IL-6 in the THP-1 cells in a dose- and time-dependent manner. TNF-α and IL-6 levels peaked at 24 h after GST-Cpn 0810 stimulation. Furthermore, GST-Cpn 0810 significantly promoted the apoptosis of THP-1 cells. In conclusion, recombinant GST-Cpn 0810 was shown to stimulate the expression of TNF-α and IL-6, inhibit proliferation and induce apoptosis in THP-1 cells. Therefore, Cpn 0810 may interact with host cells following C. pneumoniae infection, functioning as an important pathogenic factor.

[Induction of proinflammatory cytokines and cell apoptosis by Chlamydia pneumoniae Cpn0810].

AIM: To expresse the Chlamydia pneumoniae Cpn0810 in E.coli BL21, and to study weather could it inducing proinflamatory cytokines including TNF-α and IL-6 in human monocytic (THP-1) and cell apoptosis. METHODS: Polymerase chain reaction(PCR) was used to amplify the Cpn0810 gene, PCR products were purified and cloned into the prokaryotic expression vector pGEX6p-2. The restriction plasmids pGEX6p-2/Cpn0810 confirmed by PCR and sequencing was transformed into E.coli BL21. The recombinant protein was purified with glutathione S-transferase (GST) resin chromatography of Novagen after renaturation. THP-1 cells were stimulated by different concentrations of Cpn0810 and for various durations to test the production and the expression of TNF-α and IL-6 by ELISA. Cell apoptosis was detected in C.pneumoniae Cpn0810 cells by Hoechst33258 fluorescence staining and Cell apoptosis was detected in THP-1 cells by Annexin-V-FITC-propidiu-m iodide (PI) staining. RESULTS: The restriction enzymes cleavage analysis and nucleotide sequencing showed the target gene was successfully inserted into pGEX6p-2 prokaryotic expression vector. Cpn0810 stimulated THP-1 cell to produce proinflamatory cytokines including TNF-α and IL-6 in a dose and time-dependent manner. After THP-1 cells were treated with 10 mg/L Cpn0810 for 24 h, apoptosis with nuclear chromatin fragmentation as well as cell shrinkage was observed by fluorescent staining and microscopy; apoptosis of cell was detected after 24 h in THP-1 cells treated with Cpn0810. CONCLUSION: Cpn0810 recombinant protein could stimulate THP-1 cell to produce and express proinflamatory cytokines including TNF-α and IL-6; After THP-1 cells were treated with 10 mg/L Cpn0810 for 24 h, apoptosis of cell was detected after 24 h in THP-1 cells treated with Cpn0810.

Production of proinflammatory cytokines in the human THP-1 monocyte cell line following induction by Tp0751, a recombinant protein of Treponema pallidum.

The tissue destruction characteristic of syphilis infection may be caused by inflammation due to Treponema pallidum and the ensuing immune responses to the pathogen. T. pallidum membrane proteins are thought to be potent inducers of inflammation during the early stages of infection. However, the actual membrane proteins that induce inflammatory cytokine production are not known, nor are the molecular mechanisms responsible for triggering and sustaining the inflammatory cascades. In the present study, Tp0751 recombinant protein from T. pallidum was found to induce the production of proinflammatory cytokines, including TNF-alpha, IL-1beta and IL-6, in a THP-1 human monocyte cell line. The signal transduction pathways involved in the production of these cytokines were then further investigated. No inhibition of TNF-a, IL-1beta, or IL-6 production was observed following treatment with the SAPK/JNK specific inhibitor SP600125 or with an ERK inhibitor PD98059. By contrast, anti-TLR2 mAb, anti-CD14 mAb, and the p38 inhibitor SB203580 significantly inhibited the production of all three cytokines. In addition, pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of NF-kappaB, profoundly inhibited the production of these cytokines. Tp0751 treatment strongly activated NF-kappaB, as revealed by Western blotting. However, NF-kappaB translocation was significantly inhibited by treatment with PDTC. These results indicated that TLR2, CD14, MAPKs/p38, and NF-kappaB might be implicated in the inflammatory reaction caused by T. pallidum infection.

[Diagnostic and therapeutic status of benign prostatic hyperplasia outpatients at department of geriatrics in China].

OBJECTIVE: To assess the diagnostic and therapeutic modality preferences of physician implementation of the Chinese Clinical Practice Guidelines for Benign Prostatic Hyperplasia (BPH) for geriatric BPH patients. METHODS: This cross-sectional survey was conducted at 33 medical centers located in 11 different cities in China (4 in north; 7 in south). A total of 190 physicians were requested to record their preferences in diagnostic tests and treatment options for elderly BPH cases. RESULTS: The physician response rate was 97.4%. Respondents generally selected those practices consistent with the guidelines, but their preferences for recommended tests varied. The use of medical history, ultrasonography and urinalysis was higher (> 90.0%) and that of uroflowmetry was lower (31.2%). In addition, the rate of use of recommended tests was higher among physicians in the north than those in the south. Drug therapy was the preferred treatment option. The proportion of drug treatment increased with the severity of symptoms in elder patients. In the south, the proportion of drug treatment in severe cases increased to 82.6% versus 61.9% in mild cases. In the north, the proportion of rug treatment in severe cases increased to 83.5% versus 54.6% in mild cases. CONCLUSION: This study provides insights into the physician preferences of diagnosis and treatment. The physicians generally comply with the BPH clinical practice guidelines. It may also serve as a practical reference for updating and improving the Chinese Clinical Practice Guidelines for BPH.

An increase in intracelluar free calcium ions modulated by cholinergic receptors in rat facial nucleus.

BACKGROUND: Ca(2+) in the central nervous system plays important roles in brain physiology, including neuronal survival and regeneration in rats with injured facial motoneurons. The present research was to study the modulations of intracellular free Ca(2+) concentrations by cholinergic receptors in rat facial nucleus, and the mechanisms of the modulations. METHODS: The fluorescence intensity of facial nucleus in Fluo-3 AM loaded acute brainstem slices was detected by applying intracellular free Ca(2+) measurement technique via confocal laser scanning microscope. The changes of fluorescence intensity of facial nucleus indicate the average changes of intracellular free Ca(2+) levels of the neurons. RESULTS: Acetylcholine was effective at increasing the fluorescence intensity of facial nucleus. Muscarine chloride induced a marked increase of fluorescence intensity in a concentration dependent fashion. The enhancement of fluorescence intensity by muscarine chloride was significantly reduced by thapsigargin (depletor of intracellular Ca(2+) store; P < 0.01), rather than Ca(2+) free artifical cerebrospinal fluid or EGTA (free Ca(2+) chelator; P > 0.05). And the increase of fluorescence intensity was also significantly inhibited by pirenzepine (M(1) subtype selective antagonist; P < 0.01) and 4-DAMP (M(3) subtype selective antagonist; P < 0.01). In addition, fluorescence intensity was markedly increased by nicotine. The enhancement of fluorescence intensity by nicotine was significantly reduced by EGTA, nifedipine (L-type voltage-gated Ca(2+) channel blocker), dihydro-beta-erythroidine (alpha4beta2 subtype selective antagonist), and in Ca(2+) free artificial cerebrospinal fluid (P < 0.01), but not in the presence of mibefradil (M-type voltage-gated Ca(2+) channel blocker) or thapsigargin (P > 0.05). CONCLUSIONS: The data provide the evidence that muscarinic receptors may induce the increase of intracellular free Ca(2+) levels through the Ca(2+) release of intracellular Ca(2+) stores, in a manner related to M(1) and M(3) subtypes of muscarinic receptors in rat facial nucleus. Nicotine may increase intracellular free Ca(2+) concentrations via the influx of extracellular Ca(2+)+ mainly across L-type voltage-gated Ca(2+) channels, in a manner related to the alpha4beta2 subtype of nicotinic receptors.

[Incidence and natural history of middle ear disease in newborns and infants with cleft palate].

OBJECTIVE: The aim of this study is to investigate the incidence and natural history of secretory otitis media(SOM) and hearing loss in newborns and infants with cleft palate, consequently, define its audiological criteria and to predict SOM early. METHOD: Seventy-three newborns and infants with a cleft palate (146 ears) were monthly estimated by tympanogram, static compliance, acoustic stapedius reflex and auditory brainstem response (ABR) under natural sleep within one year of age. RESULT: Au the infants with cleft palate had the suspected SOM in the first 6 months of life. Among children with cleft palate, the suspected SOM were most prevalent in the 3-month-age. 78. 8% infants with cleft palate had the confirmed SOM in the first 12 months of life. SOM were most prevalent in the 6-month-age. The SOM prodromal period was averagely 3. 8 months from suspected SOM to confirmed SOM. 56. 2% infants with cleft palate had a conductive hearing loss in the first 12 months of life. The conduction hearing thresholds of ABR (2-4 Hz) were averagely 48. 6 dBnHL. CONCLUSION: The highest incidence of SOM and hearing loss in children with cleft palate appear in infants in the first 1 year of life. The process of SOM and hearing loss onset is progressive process. The infants with cleft palate should be estimated by ABR and acoustic immittance audiometry in each period of 2 or 3 months after birth.

[The expression of intercellular adhesion molecule-1 and interleukin-6 in nasal and bronchial mocosa in allergic rhinitis].

OBJECTIVE: To investigate the expression and its significances of intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in nasal and bronchial mocosa in allergic rhinitis. METHOD: Samples of nasal and bronchial mucosa were from 28 patients with allergic rhinitis and 12 controls and their paraffin sections were studied with immuno histochemical technique staining with ICAM-1 monoclonal antibodies and IL-6 polyclonal antibodies. RESULT: The positive expression percentage of ICAM-1 in mucosa of nasal and bronchial in patients with allergic rhinitis were 100% and 92.86%. No difference were observed between them, P>0.05. But in the group of controls, those were obviously lower (66.67% and 58.33%). The difference between them was significant, P<0.05. The positive expression percentage of IL-6 in mucosa of nasal and bronchial in patients with allergic rhinitis were 100% and 82.14%. No difference were observed between them, P>0.05. But in the group of normal controls, those were obviously lower (41.67% and 41.67%). The difference between them was significant, P<0.05. CONCLUSION: ICAM-1 and IL-6 are important cytokines in the allergic inflammation in airway. The closely correlation was observed between the allergic inflammation in upper and lower airway, so that the upper and lower airway should be treated as a united one. To otorhinolaryngologists and respiratory doctors, it is safe and efficient treatment to treat the inflammatory diseases in upper and lower airway at the same time.

[Relationship between levels of intercellular adhesion molecule-1, interleukin-6 and airway hyperresponsiveness in patients with allergic rhinitis].

OBJECTIVE: To investigate the relation between levels of intercellular adhesion molecule-1, interleukin-6 and airway hyperresponsiveness in patients with allergic rhinitis. METHODS: Fifty-four patients with allergic rhinitis (AR) and 20 controls were included in the study. The levels of intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in nasal lavage fluid, gathered 1 hour after specific allergen nasal provocation test (SANPT), were detected by sandwich enzyme-linked immunosorbent assay (ELISA) technique. The pulmonary function (FEV1) and nonspecific bronchial provocation test were measured in 54 patients with AR, 36 patients with AR and bronchial asthma (BA) and 20 controls. At the same time, the correlation between levels of ICAM-1 and IL-6 in nasal lavage fluid and pulmonary function (FEV1) was studied. RESULTS: The levels of ICAM-1 and IL-6 in nasal lavage fluid from patients with AR were (272.75 +/- 32.25) pg/ml and (52.11 +/- 16.54) pg/ml, significantly higher than those the controls, which were (158.82 +/- 33.88) pg/ml and (25.64 +/- 10.14) pg/ml (P < 0.01). The pulmonary function (FEV1) in patients with AR and BA was (78.82 +/- 7.41)%. It was obviously lower than that in patients with AR [(83.90 +/- 4.87)%], much lower than that in normal controls [(90.25 +/- 4.69)%]. The difference among them was significant. In patients with AR, the positive percentage of bronchial provocation test was 64.81%, in patients with AR and BA, it was 83.33% in normal controls, it was 0. The differences among them had very significant meaning. The levels of ICAM-1 and IL-6 in nasal provocation fluid had closely negative correlation with pulmonary function (FEV1), r = -0.7071, -0.6248, P < 0.01. CONCLUSIONS: The close correlation was observed in upper and lower airway for allergic inflammation. The pulmonary function of patients with AR was lower, and 64. 8% of them had airway hyperresponsiveness, so that they had the potent possibility to have bronchial asthma.

[Evaluation of healing effect for simultaneously tympanoplasty in treating chronic suppurative otitis media with cholesteatoma and/or granulation tissue].

OBJECTIVE: This study was designed to discuss possibility and factors influencing healing effect for simultaneously tympanoplasty of chronic suppurative otitis media with cholesteatoma and/or granulation tissue. METHOD: For 52 cases with chronic suppurative otitis media with cholesteatoma (30 ears) and/or granulation tissue (22 ears), cleaning lesion with simultaneously tympanoplasty was surgical procedure, among them, 12 ears treated with single tympanoplasty, 40 ears treated with mastoidectomy and tympanoplasty. RESULT: All cases had dry ears without recurring cholesteatoma. Among them, hearing of 5 patients improved more than 30 dB, 9 ears improved from 20 to 29 dB, 31 ears improved from 10 to 19 dB and 7 ears improved less than 10 dB. Hearing of no cases reduced than that in preoperation. CONCLUSION: Simultaneously tympanoplasty would be carried out possible in treating chronic suppurative otitis media with cholesteatoma and/or granulation tissue. There were two important factors influencing hearing improvement, which concluded effective area of tympanic membrane concussion, activity of stapes and/or stapes footplate. The main cause for failure in hearing improvement would be eustachian tube obstruction.