Objectives: This study aimed to assess the antibacterial, bactericidal, and mouth freshener effects of lysozyme hydrochloride 0.01%, sodium fluoride 0.02%, and cetylpyridinium chloride 0.05%. Methods: Eight oral disease-related bacteria were cultivated anaerobically. Four samples were prepared with or without 0.5% cetylpyridinium chloride, 0.2% sodium fluoride, and 0.1% lysozyme hydrochloride. Antimicrobial activity was tested in 96-well microplates. After assessing the bacterial count, the bacterial suspension was mixed with samples and spread on agar. The bactericidal rate was calculated by counting and comparing treated and untreated colonies. Results: Lysozyme hydrochloride 0.01%, sodium fluoride 0.02%, and cetylpyridinium chloride 0.05% mouth fresheners sterilized 99.99% of 8 oral bacteria, including Streprococcus mutans. Lysozyme hydrochloride 0.01%, sodium fluoride 0.02%, and cetylpyridinium chloride 0.05% mouth fresheners showed 99.97% bactericidal activity against Lactobacillus acidophilus. Conclusions Lysozyme hydrochloride 0.01%, sodium fluoride 0.02%, and cetylpyridinium chloride 0.05% mouth fresheners confirmed the sterilization and antibacterial effects on oral disease-causing bacteria.

Objectives: To investigate the effect of nicotine on the healing of an oral cavity wound, high and low concentrations of nicotine were administered on human gingival fibroblasts. Methods: Nicotine at concentrations of 0.1, 1, 5, and 10 mM were administered to gingival fibroblasts to evaluate the survival capability of the cells. Nicotine at 0.1 mM, a nonapoptotic concentration, was administered to evaluate apoptosis using Annexin V-FITC/Propidium Iodide cell staining.Nicotine at 1, 10, and 100 mM were administered to measure the expression of inflammatory cytokines, which was measured by RT-PCR and ELISA. FGF was treated with an additional 1, 10, or 100 mM of nicotine to evaluate cell proliferation and wound healing. Results: As the concentration of nicotine increased (0.1, 1, 5, and 10 mM), the survival capability of the cells reduced. When cells were exposed to low nicotine concentration (0.1 mM) for 24 h, apoptosis occurred. Moreover, if the cell was exposed for 48 h, cell apoptosis occurred with necrosis. As the concentration of nicotine increased (1, 10, and 100 mM), more inflammatory cytokines were expressed. When EC LPS and TF LPS were combined with a low concentration of nicotine (1 and 10 mM), the expression of inflammatory cytokines was suppressed. The FGF level decreased as the nicotine concentration increased (1, 10, and 100 mM). Conclusions Nicotine interferes with the wound healing process of gingival fibroblasts. To maintain the wound healing process after a surgery or dental procedure, cessation of smoking is recommended.

PURPOSE: To determine treatment protocol for inoperable esophageal cancer patients, we evaluated survival rate and prognostic factors. MATERIALS AND METHODS: We evaluated esophageal cancer treated by curative or palliative aim in KCCH from 1992 to 1996, retrospectively. Recurrent or underdose case below 40 Gy were excluded. The number of male and female were 35 and 5, respectively. Thirty-eight patients were squamous carcinoma and 2 patients were not biopsy proven. Ten patients were treated with radiation therapy and chemotherapy. Median dose of radiation therapy was 59.4 Gy and the range was 40-60 Gy. RESULTS:The median survival is 6.5 months and 1-year survival rate was 28.3%. Age, location, radiation dose and chemotherapy were not significant prognostic factors. Median survivals of patients with below stage III and over stage IVA were 7.6 and 6.2 months respectively, but it is not significant. CONCLUSION:The survival for esophageal cancer is very poor. For patients with curative aim, chemotherapy must be considered. For patients with palliative aim, short-term external beam radiation therapy and/or brachytherapy must be considered.
Biopsy ; Brachytherapy ; Carcinoma, Squamous Cell ; Clinical Protocols ; Drug Therapy ; Esophageal Neoplasms ; Female ; Humans ; Male ; Retrospective Studies ; Survival Rate

Cicatrix ; Follow-Up Studies ; Genioplasty ; Humans ; Incidence ; Intention ; Mandible ; Mandibular Nerve ; Mouth ; Nerve Fibers ; Neural Conduction ; Osteotomy ; Osteotomy, Sagittal Split Ramus ; Prognathism ; Retrognathia

In thyroid hormone resistance syndrome (THR) TSH levels are normal or elevated despite thyroid hormone levels being elevated. THR is distinguished from TSH-producing pituitary adenoma by TRH stimulation and alpha-subunit tests, thyroid hormone receptor (TR) beta gene analysis, and sellar MRI. A 24-year old man with diffuse goiter visited our hospital complaining of fatigue, heat intolerance, palpitation, and weight loss. He had elevated total T3 and free T4 levels, but normal TSH levels. Serum TSH levels during TRH stimulation tests performed before and after T3 suppression showed normal and non-suppressible responses, respectively. The serum basal alpha-subunit test result was normal. A TR beta gene R438H mutation was identified, and a pituitary mass with cystic change was identified by sellar MRI. We report a case of THR with a mutation (R438H) in the TR beta gene, the first case of its kind in Korea.
Fatigue ; Genes, erbA ; Goiter ; Hot Temperature ; Korea ; Pituitary Neoplasms ; Receptors, Thyroid Hormone ; Thyroid Gland ; Thyroid Hormone Receptors beta ; Thyroid Hormone Resistance Syndrome ; Weight Loss

This study evaluated the effect of a combination of acetaminophen and vitamin C (CAV) on reducing serum cortisol and tumor necrosis factor-α (TNF-α) concentrations in piglets vaccinated with foot-and-mouth disease (FMD) vaccine. Piglets were vaccinated with FMD vaccine and treated with CAV at concentrations of 0.0, 0.5, 1.0, and 2.0 kg/ton feed (P-CON, AD-1, AD-2, and AD-3, groups, respectively) for 5 days post-vaccination. Cortisol and TNF-α levels at 5 days post-treatment in the AD-1–3 groups were significantly lower than that in the P-CON group (p < 0.05). There were no significant differences between AD-2 and AD-3 groups and non-vaccinated, non-CAV-treated piglets.
Acetaminophen* ; Animals ; Ascorbic Acid* ; Foot-and-Mouth Disease* ; Hydrocortisone* ; Necrosis ; Swine* ; Tumor Necrosis Factor-alpha* ; Vitamins*

BACKGROUND: The therapeutic effects of surfactant on acute lung injury derive not only from its recruiting action on collapsed alveoli but also from its anti-inflammatory effects. Pro-apoptotic action on alveolar neutrophils represents one of the important anti-inflammatory mechanisms of surfactant. In the present study, we evaluated the effects of surfactant on the apoptosis of human peripheral and rat alveolar neutrophils. METHODS: In the (Ed- the article is not definitely needed but it helps to separate the two prepositions 'in') in vitro study, human neutrophils were collected from healthy volunteers. An equal number of neutrophils (1X10(6)) (Ed-confirm) was treated with LPS (10, 100, 1000ng/ml), surfactant (10, 100, 1000micro gram/ml), or a combination of LPS (1000ng/ml) and surfactant (10, 100, 1000micro gram/ml). After incubation for 24 hours, the apoptosis of neutrophils was evaluated by Annexin V method. In the in vivo study, induction of acute lung injury in SD rats by intra-tracheal instillation of LPS (5mg/kg) was followed by intra-tracheal administration of either surfactant (30mg/kg) or normal saline (5ml/kg). Twenty-four hours after LPS instillation, alveolar neutrophils were collected and the apoptotic rate was evaluated by Annexin V method. In addition, changes of the respiratory mechanics of rats (respiratory rate, tidal volume, and airway resistance) were evaluated with one chamber body plethysmography before, and 23 hours after, LPS instillation. RESULTS: In the in vitro study, LPS treatment decreased the apoptosis of human peripheral blood neutrophils (control; 47.4+/-5.0%, LPS 10ng/ml; 30.6+/-10.8%, LPS 100ng/ml; 27.5+/-9.5%, LPS 1000ng/ml; 24.4+/-7.7%). The combination of low to moderate doses of surfactant with LPS promoted apoptosis (LPS 1000ng/ml + Surf 10micro gram/ml; 36.6+/-11.3%, LPS 1000ng/ml + Surf 100micro gram/ml; 41.3+/-11.2%). The high dose of surfactant (1000micro gram/ml) decreased apoptosis (24.4+/-7.7%) and augmented the anti-apoptotic effect of LPS (LPS 1000ng/ml + Surf 1000micro gram/ml; 19.8+/-5.4%). In the in vivo study, the apoptotic rate of alveolar neutrophils of surfactant-treated rats was higher than that of normal saline-treated rats (6.03+/-3.36% vs. 2.95+/-0.58%). The airway resistance (represented by Penh) of surfactant-treated rats was lower than that of normal saline-treated rats at 23 hours after LPS injury (2.64+/-0.69 vs. 4.51+/-2.24, p<0.05). CONCLUSIONS: Surfactant promotes the apoptosis of human peripheral blood and rat alveolar neutrophils. Pro-apoptotic action on neutrophils represents one of the important anti-inflammatory mechanisms of surfactant.
Acute Lung Injury* ; Airway Resistance ; Animals ; Annexin A5 ; Apoptosis* ; Healthy Volunteers ; Humans ; Neutrophils* ; Plethysmography ; Rats* ; Respiratory Mechanics ; Tidal Volume

We reported a case of complicated silicosis that occurred in a glass manufacturing plant worker who had presumably been exposed to low-concentration free silica for almost 20 years. To the best of our knowledge this report is the first in the Republic of Korea. The physician's first impression was cancer since the enlargement of neck and supraclavicuar lymph nodes had clearly progressed and metastasis was suspected in ultrasonography. However, it turned out to be reactive hyperplasia and anthracosis. Although lung cancer was suspected and tests were performed in 2 hospitals due to repetitive cough and dyspnea, along with weight loss of approximately 10% over the course of 7 months, the patient was eventually diagnosed with complicated silicosis and pneumothorax occurred after 1 year. Herein, we report this case with a literature review.
Anthracosis ; Cough ; Dyspnea ; Glass* ; Humans ; Hyperplasia ; Lung Neoplasms ; Lymph Nodes ; Neck ; Neoplasm Metastasis ; Plants ; Pneumothorax ; Republic of Korea ; Silicon Dioxide ; Silicosis* ; Ultrasonography ; Weight Loss

Bronchial asthma is a chronic airway inflammation disorder involving lymphocyte activation and various cytokines secretion by lymphocyte. The inflammatory response results from a complex network of interactions between inflammatory cells (mast cells, eosinophils, macrophages) and resident cells belonging to the lung structure itself like EC, fibroblasts, or bronchial epithelial cells. IL-6 which is known to up-regulate the endothelial cell expression of adhesion molecules participating in the development of the inflammatory reaction in bronchial asthma is produced by alveolar macrophage. ICAM-1 is produced by bronchial epithelial cell and expression by endothelial cell, which is known to enhance of the influx of various cells. RANTES which is known to a potent chemoattractant for eosinophils, lymphocytes, and monocytes, a member of the CC chemokine family, is expressed by bronchial epithelial cell. To evaluate whether markers of lymphocyte activation are useful markers of disease activity in bronchial asthma, we measured sIL-6, sICAM-1, sRANTES in 42 patients with mild to moderate bronchial asthma and in 26 normal controls and compared the result with other disease activity markers in asthma (pulmonary function, blood eosinophil counts). The mean level of sIL-6 was higher than that of normal control and correlated significantly with sICAM-1, FEV1% to predicted value. The mean level of sICAM-1 was higher than that of normal control and correlated significantly with FEV1%, FEV1% to predicted value. The mean level of sRANTES showed the tendency to be higher than that of normal control, but not significant statistically, and did not correlated with sIL-6, sICAM-1, FEV1%, FEV1% to predicted value, blood eosinophil counts. It appeared that sIL-6 and sICAM-1 could be a disease marker in bronchial asthma. But, clinical application of the measurement of these markers needs to be studied further.
Asthma* ; Chemokine CCL5 ; Cytokines ; Endothelial Cells ; Eosinophils ; Epithelial Cells ; Fibroblasts ; Humans ; Inflammation ; Intercellular Adhesion Molecule-1 ; Interleukin-6 ; Lung ; Lymphocyte Activation ; Lymphocytes ; Macrophages, Alveolar ; Monocytes

PURPOSE: Pancreatic acinar cell carcinoma (ACC) is a rare cancer of the exocrine pancreas. Because of its rare incidence, the efficacy of chemotherapy in this patient population has been largely unknown. Therefore, we retrospectively analyzed the outcomes of patients with advanced pancreatic ACC who received chemotherapy. MATERIALS AND METHODS: Between January 1997 and March 2015, 15 patients with unresectable or metastatic pancreatic ACC who received systemic chemotherapy were identified in Asan Medical Center, Korea. RESULTS: The median age was 58 years. Eleven and four patients had recurrent/metastatic and locally advanced unresectable disease. The median overall survival in all patients was 20.9 months (95% confidence interval [CI], 15.7 to 26.1). As first-line therapy, intravenous 5-fluorouracil were administered in four patients (27%), gemcitabine in five (33%), gemcitabine plus capecitabine in two (13%), oxaliplatin plus 5-fluorouracil/leucovorin (FOLFOX) in two (13%), and concurrent chemoradiotherapy followed by capecitabine maintenance therapy in two (13%). The objective response rate (ORR) to chemotherapy alone was 23% and the median progression-free survival (PFS) was 5.6 months (95% CI, 2.8 to 8.4). After progression, second-line chemotherapy was administered in eight patients, while four patients received FOLFOX and the other four patients received gemcitabine. The ORR was 38%, and patients administered FOLFOX had significantly better PFS than those administered gemcitabine (median, 6.5 months vs. 1.4 months; p=0.007). The ratio of time to tumor progression (TTP) during first-line chemotherapy to TTP at second-line chemotherapy was significantly higher in patients administered FOLFOX (4.07; range, 0.87 to 8.30) than in those administered gemcitabine (0.12; range, 0.08 to 0.25; p=0.029). CONCLUSION: Our results suggest that oxaliplatin-containing regimens may have improved activity against pancreatic ACC.
Acinar Cells* ; Antineoplastic Agents ; Capecitabine ; Carcinoma, Acinar Cell* ; Chemoradiotherapy ; Chungcheongnam-do ; Disease-Free Survival ; Drug Therapy* ; Fluorouracil ; Humans ; Incidence ; Korea ; Pancreas, Exocrine ; Pancreatic Neoplasms ; Retrospective Studies