A Clinical Approach for the Removal of a Large Antral Pseudocyst with Simultaneous Maxillary Sinus Augmentation: A Case Series.

For a large benign lesion within the maxillary sinus, such as an antral pseudocyst, maxillary sinus floor augmentation is more commonly performed using a two-stage approach. This involves first removing the lesion, and then, re-entry following several months of healing. In this case series, we described the "one-bony-window" approach, which is a technical surgical modification of the previous one-stage approach, for simultaneous cyst removal and maxillary sinus floor augmentation. Four patients with large maxillary antral pseudocysts were included. The "one-bony-window" approach involves the preparation of a large window opening of approximately 15 mm × 20 mm at the lateral wall. A mesiodistally extended intentional perforation was made in the upper part of the exposed membrane to enhance the access for instrumentation. The antral pseudocyst was removed in its entirety without being deformed to prevent rupture or leakage of the cystic contents. Subsequent detachment and elevation of the Schneiderian membrane at the sinus floor significantly reduced the perforation site, and bone grafting with implant placement was performed simultaneously. This alleviated the need to surgically repair the perforation. The lateral opening was either uncovered or repositioned using bony window lids. Healing abutments were connected after six months, and the final prosthesis was placed after two months. At the 1-year follow-up, the antral pseudocysts had resolved with no specific recurrence, and the stability of the augmented sinus was maintained with excellent implant survival. Within the limitations of our findings, the "one-bony-window" technique can be suggested for the simultaneous removal of large antral pseudocysts and maxillary sinus floor augmentation with favorable clinical outcomes.

Comparative effectiveness of budesonide inhalation suspension and montelukast in children with mild asthma in Korea.

Objective: The comparative effectiveness of low-dose budesonide inhalation suspension (BIS) versus oral montelukast (MON) in managing asthma control among children with mild asthma was assessed in Korea.Methods: Claims from Korea's national health insurance database for children (2-17 years) with mild asthma (GINA 1 or 2) who initiated BIS or MON during 2015 were retrospectively analyzed. Pre- and post-index windows were 1 year each. Adherence, persistency, asthma control, asthma-related health-care resource utilization, and costs were evaluated using unadjusted descriptive statistics and propensity score-matched regression analyses.Results: The number of children identified was 26,052 for unmatched (n = 1,221 BIS; n = 24,831 MON) and 2,290 for matched populations (n = 1,145 per cohort). Medication adherence, measured by proportion of days covered, was low for both cohorts but significantly higher for MON versus BIS (13.8% vs. 4.5%; p < .001). Time to loss of persistency was longer for MON versus BIS (82.3 vs. 78.4 days, respectively; p < .001). Mean number of post-index asthma-related office visits was 6.6 for BIS versus 8.3 for MON (p < .001). However, a greater proportion of patients in the BIS cohort had an asthma exacerbation-related office visit than the MON cohort (78.3% vs. 56.1%; p < .001). Asthma-related total health-care costs were higher with MON versus BIS (₩ 190,185 vs. ₩ 167,432, respectively; p < .001), likely driven by higher pharmaceutical costs associated with MON (₩ 69,113 vs. ₩ 49,225; p < .001).Conclusions: Montelukast patients had better adherence, a longer time to loss of persistency, and were less likely to experience an exacerbation-related office visit in the post-index period than BIS patients.

Antifibrotic Effects of Sakuraso-Saponin in Primary Cultured Pterygium Fibroblasts in Comparison With Mitomycin C.

Purpose: To investigate the antifibrotic effects of sakuraso-saponin on a primary culture of human pterygium fibroblasts (HPFs) and normal human Tenon fibroblasts (HTFs) as compared to the effects of mitomycin C (MMC). Methods: Samples of HPFs and HTFs were acquired during primary pterygium surgery. Cell toxicity, cell migration, and expression of α-smooth muscle actin (α-SMA) and transforming growth factor-ß (TGF-ß) were evaluated in HPFs and HTFs after treatment with sakuraso-saponin and MMC. To determine the possible mechanisms underlying the antifibrotic effects of sakuraso-saponin, the expression of phosphorylated Smad2/3 was evaluated after treatment with sakuraso-saponin and MMC. Results: MMC (≥200 µg/mL) significantly reduced cell viability in both HPFs and HTFs, whereas sakuraso-saponin (1.0 µg/mL) decreased cell viability in HPFs only. Both sakuraso-saponin (1.0 µg/mL) and MMC (200 µg/mL) treatment significantly reduced the expression of α-SMA and TGF-ß in HPFs (P < 0.05). It is interesting that the expression of α-SMA and TGF-ß after treatment with sakuraso-saponin was significantly lower than that after treatment with MMC (P < 0.05). The expression of phosphorylated Smad2/3 protein was decreased by sakuraso-saponin and MMC in HPFs. Both sakuraso-saponin and MMC inhibited TGF-ß1-induced cell migration as compared to the control in HPFs. Conclusions: Sakuraso-saponin could be more effective than MMC for the reduction of fibrosis in HPFs. Our results might present the basis for its use as a promising candidate drug for adjuvant therapy to prevent recurrent pterygium after surgery.

Effect of nerve growth factor on the in vitro induction of apoptosis of human conjunctival epithelial cells by hyperosmolar stress.

PURPOSE: To evaluate the effects of nerve growth factor (NGF), which is activated during inflammatory episodes of ocular diseases, on the apoptotic response in cultured human primary conjunctival epithelial cells (pHCECs). METHODS: Levels of NGF transcripts and NGF protein in pHCEC grown in medium with normal osmolarity (307 mOsm/L) or hyperosmolar medium (350, 400, and 450 mOsm/L) were determined using RT-PCR or ELISA, respectively. To assess apoptosis, pHCEC were cultured in normal or 400 mOsm/L hyperosmolar medium with neutralizing anti-NGF antibody or recombinant human NGF for 6 hours before analysis by flow cytometry. Levels of Bcl-xL, Bax, phosphorylated JNK, and cleaved caspase-3 were detected using Western blotting. Levels of the inflammatory cytokine IL-6 was analyzed using ELISA. RESULTS: Hyperosmolar conditions increased NGF levels in cultured pHCECs. Hyperosmolarity and exposure to neutralizing anti-NGF antibody significantly increased the number of apoptotic cells. Addition of recombinant human NGF to 400 mOsm/L medium decreased the number of apoptotic cells, reduced the expression of phosphorylated JNK, Bax, and cleaved caspase-3 and increased the expression of Bcl-xL. Levels of IL-6 were increased by hyperosmotic stress but decreased by exposure to recombinant human NGF. CONCLUSIONS: Hyperosmolarity induces apoptosis of pHCECs by activating JNK signaling. Increased levels of NGF under hyperosmolar conditions may contribute, at least in part, to the reduced apoptosis of pHCECs and may be beneficial in recovering conjunctival damage due to chronic hyperosmolar stress.

A novel glucosamine derivative exerts anti-inflammatory actions via inhibition of nuclear factor-kappaB.

Glucosamine suppresses lipopolysaccharide (LPS)-induced upregulation of pro-inflammatory mediators both in vivo and in culture systems of mouse microglia or macrophage. In the present study, we show that the novel glucosamine derivative, 2-deoxy-2-[(o-methylbenzylidene)]-ß-glucopyranoside (NK-4), significantly reduced LPS-induced production of nitric oxide (NO) in BV2 microglia, RAW264.7 macrophage, and primary cultured peritoneal macrophages cells. NK-4 inhibited LPS-induced upregulation of inducible NO synthase (iNOS), cyclooxygenase-2, interleukin-6, tumor necrosis factor-α, and interleukin-1ß in RAW264.7 cells in a time- and concentration-dependent manner. Furthermore, administering NK-4 significantly inhibited the induction of inflammatory cytokine mRNAs in the brains of LPS-injected mice. Although NK-4 inhibited LPS-induced nuclear factor-kappaB (NF-κB) activation, IκB-α degradation was not changed. Instead, NK-4 inhibited LPS-induced DNA-binding activity of NF-κB by suppressing p50 and c-Rel binding to NF-κB binding site of the iNOS promoter.

Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury.

We investigated the neuroprotective effect of glucosamine (GlcN) in a rat middle cerebral artery occlusion model. At the highest dose used, intraperitoneal GlcN reduced infarct volume to 14.3% ± 7.4% that of untreated controls and afforded a reduction in motor impairment and neurological deficits. Neuroprotective effects were not reproduced by other amine sugars or acetylated-GlcN, and GlcN suppressed postischemic microglial activation. Moreover, GlcN suppressed lipopolysaccharide (LPS)-induced upregulation of proinflammatory mediators both in vivo and in culture systems using microglial or macrophage cells. The anti-inflammatory effects of GlcN were mainly attributable to its ability to inhibit nuclear factor kappaB (NF-κB) activation. GlcN inhibited LPS-induced nuclear translocation and DNA binding of p65 to both NF-κB consensus sequence and NF-κB binding sequence of inducible nitric oxide synthase promoter. In addition, we found that GlcN strongly repressed p65 transactivation in BV2 cells using Gal4-p65 chimeras system. P65 displayed increased O-GlcNAcylation in response to LPS; this effect was also reversed by GlcN. The LPS-induced increase in p65 O-GlcNAcylation was paralleled by an increase in interaction with O-GlcNAc transferase, which was reversed by GlcN. Finally, our results suggest that GlcN or its derivatives may serve as novel neuroprotective or anti-inflammatory agents.

Anodic oxidation of 1,4-dioxane on boron-doped diamond electrodes for wastewater treatment.

A study of the anodic oxidation of 1,4-dioxane, a refractory water pollutant, by boron-doped diamond (BDD) electrodes was carried out under a range of major system variables: initial concentration, current density, temperature, pH, and electrolyte concentration. The 1,4-dioxane removal behavior was monitored by chemical oxygen demand (COD), and the results were compared with theoretical models for the electrochemical incineration of organic compounds. The removal efficiency of COD was shown to be greater than 95% in most cases, and no electrode fouling was observed during the reaction. Experimental degradation behavior agreed well with the theoretical models, implying that system variables can be predicted, even when the process is applied at pilot scale. Processes conducted at lower initial concentrations and higher temperatures yielded better energy consumption efficiency. Conditions of higher current density yielded faster degradation but need greater quantities of charge loading into the system. Therefore, a compromise between treatment time and energy consumption is required to achieve the desired efficiency. Meanwhile, pH and electrolyte concentrations did not affect reaction efficiency, suggesting that pH adjustment prior to wastewater treatment is not necessary. Thus, anodic oxidation of 1,4-dioxane by BDD electrodes promises to be both an economical and an efficient in wastewater treatment process.

Syndecan-2 regulates cell migration in colon cancer cells through Tiam1-mediated Rac activation.

Expression of the cell surface adhesion receptor syndecan-2 is known to be involved in the regulation of cancer cell migration. However, the molecular mechanism of syndecan-2-mediated cell migration remains unknown. Here we report that Rac contributes to the regulation of syndecan-2-mediated cancer cell migration. Overexpression of syndecan-2 enhanced migration and invasion of human colon adenocarcinoma cells Caco-2 and HCT116 cells. In parallel with the increased cell migration/invasion, syndecan-2 overexpression enhanced Rac activity, while dominant negative Rac (RacN17) diminished syndecan-2-mediated increased cancer cell migration. In addition syndecan-2 expression increased membrane localization of Tiam1 and syndecan-2-mediated cell migration/invasion of Caco-2 cells was diminished when Tiam1 levels were knocked-down with small inhibitory RNAs. Furthermore, oligomerization-defective syndecan-2 mutants failed to increase membrane localization of Tiam1, activation of Rac and subsequent cell migration of both Caco-2 and HCT116 cells. Taken together, these results suggest that syndecan-2 regulates cell migration of colon carcinoma cells through Tiam1-dependent Rac activation in colon cancer cells.

Induction of glioma apoptosis by microglia-secreted molecules: The role of nitric oxide and cathepsin B.

Microglia contributes significantly to brain tumor mass, particularly in astrocytic gliomas. Here, we examine the cytotoxic effects of soluble components secreted from microglia culture on glioma cells. Microglia conditioned culture medium (MCM) actively stimulated apoptotic death of glioma cells, and the effects of MCM prepared from LPS- or IFN-gamma-activated microglia were more pronounced. The cytotoxic effects were glioma-specific in that primary cultured rat astrocytes were not affected by MCM. A donor of peroxynitrite induced glioma-specific cell death. In addition, NO synthase inhibitor suppressed glioma cell death induced by activated MCM, indicating that NO is one of the key molecules responsible for glioma cytotoxicity mediated by activated MCM. However, since unstimulated resting microglia produces low or very limited level of NO, MCM may contain other critical molecule(s) that induce glioma apoptosis. To identify the proteins secreted in MCM, proteomic analysis was performed on control or activated medium. Among over 200 protein spots detected by Coomassie blue staining, we identified 26 constitutive and 28 LPS- or IFN-gamma-regulated MCM proteins. Several cathepsin proteases were markedly expressed, which were reduced upon activation. In particular, suppression of cathepsin B by the chemical inhibitors significantly reversed MCM-induced glioma cell death, implying a critical role of this protease in cytotoxicity. Our findings provide evidence on the functional implications of specific microglial-secreted proteins in glioma cytotoxicity, as well as a basis to develop a proteomic databank of both basal and activation-related proteins in microglia.