Objective: Dysphagia is a common clinical condition characterized by difficulty in swallowing. It is sub-classified into oropharyngeal dysphagia, which refers to problems in the mouth and pharynx, and esophageal dysphagia, which refers to problems in the esophageal body and esophagogastric junction. Dysphagia can have a significant negative impact one’s physical health and quality of life as its severity increases. Therefore, proper assessment and management of dysphagia are critical for improving swallowing function and preventing complications. Thus a guideline was developed to provide evidence-based recommendations for assessment and management in patients with dysphagia. Methods: Nineteen key questions on dysphagia were developed. These questions dealt with various aspects of problems related to dysphagia, including assessment, management, and complications. A literature search for relevant articles was conducted using Pubmed, Embase, the Cochrane Library, and one domestic database of KoreaMed, until April 2021. The level of evidence and recommendation grade were established according to the Grading of Recommendation Assessment, Development and Evaluation methodology. Results: Early screening and assessment of videofluoroscopic swallowing were recommended for assessing the presence of dysphagia. Therapeutic methods, such as tongue and pharyngeal muscle strengthening exercises and neuromuscular electrical stimulation with swallowing therapy, were effective in improving swallowing function and quality of life in patients with dysphagia. Nutritional intervention and an oral care program were also recommended. Conclusion This guideline presents recommendations for the assessment and management of patients with oropharyngeal dysphagia, including rehabilitative strategies.

Purpose: The treatment outcome of brentuximab vedotin (BV) has not been related with CD30 expressionin previous studies enrolling patients with a wide range of CD30 expression level.Thus, this study explored the efficacy of BV in high-CD30–expressing non-Hodgkin lymphoma(NHL) patients most likely to benefit. Materials and Methods: This phase II study (Clinicaltrials.gov: NCT02280785) enrolled relapsed or refractory high-CD30–expressing NHL, with BV administered intravenously at 1.8 mg/kg every 3 weeks.The primary endpoint was > 40% disease control rate, consisting of complete response(CR), partial response (PR), or stable disease. We defined high CD30 expression as ! 30%tumor cells positive for CD30 by immunohistochemistry. Results: High-CD30-expressing NHL patients (n=33) were enrolled except anaplastic large cell lymphoma.The disease control rate was 48.5% (16/33) including six CR and six PR; six patients(4CR, 2PR) maintained their response over 16 completed cycles. Response to BV and survivalwere not associated with CD30 expression levels. Over a median of 29.2 months offollow-up, the median progression-free and overall survival rates were 1.9 months and 6.1months, respectively. The most common adverse events were fever (39%), neutropenia(30%), fatigue (24%), and peripheral sensory neuropathy (27%). In a post-hoc analysis forthe association of multiple myeloma oncogene 1 (MUM1) on treatment outcome, MUM1-negative patients showed a higher response (55.6%, 5/9) than MUM1-positive patients(13.3%, 2/15). Conclusion BV performance as a single agent was acceptable in terms of disease control rates and toxicityprofiles, especially MUM1-negative patients.

BACKGROUND: Recent findings in molecular pathology suggest that genetic translocation and/or overexpression of oncoproteins is important in salivary gland tumorigenesis and diagnosis. We investigated PLAG1, SOX10, and Myb protein expression in various salivary gland neoplasm tissues. METHODS: A total of 113 cases of surgically resected salivary gland neoplasms at the National Cancer Center from January 2007 to March 2017 were identified. Immunohistochemical staining of PLAG1, SOX10, and Myb in tissue samples was performed using tissue microarrays. RESULTS: Among the 113 cases, 82 (72.6%) were benign and 31 (27.4%) were malignant. PLAG1 showed nuclear staining and normal parotid gland was not stained. Among 48 cases of pleomorphic adenoma, 29 (60.4%) were positive for PLAG1. All other benign and malignant salivary gland neoplasms were PLAG1-negative. SOX10 showed nuclear staining. In normal salivary gland tissues SOX10 was expressed in cells of acinus and intercalated ducts. In benign tumors, SOX10 expression was observed in all pleomorphic adenoma (48/48), and basal cell adenoma (3/3), but not in other benign tumors. SOX10 positivity was observed in nine of 31 (29.0%) malignant tumors. Myb showed nuclear staining but was not detected in normal parotid glands. Four of 31 (12.9%) malignant tumors showed Myb positivity: three adenoid cystic carcinomas (AdCC) and one myoepithelial carcinoma with focal AdCC-like histology. CONCLUSIONS: PLAG1 expression is specific to pleomorphic adenoma. SOX10 expression is helpful to rule out excretory duct origin tumor, but its diagnostic value is relatively low. Myb is useful for diagnosing AdCC when histology is unclear in the surgical specimen.
Adenoma ; Adenoma, Pleomorphic ; Antibody-Dependent Cell Cytotoxicity ; Carcinogenesis ; Carcinoma, Adenoid Cystic ; Diagnosis ; Immunohistochemistry ; Oncogene Proteins ; Oncogene Proteins v-myb ; Parotid Gland ; Pathology, Molecular ; Salivary Gland Neoplasms ; Salivary Glands ; SOX Transcription Factors ; Translocation, Genetic

Infection-associated plasmacytosis is not uncommon; however, marked plasmacytosis in both peripheral blood and bone marrow that mimicks plasma cell leukemia is a very rare condition. We encountered a case of extreme plasmacytosis associated with Klebsiella pneumoniae sepsis in an aplastic anemia patient. A 42-year-old man presented with high fever of 5 days' duration. Hematological analysis revealed severe neutropenia and thrombocytopenia; his white blood cell count was 900/mm3, with 26% of plasma and plasmacytoid cells in peripheral blood. Bone marrow biopsy and aspiration showed 25% cellularity with marked plasmacytosis (80%), highly suggestive of plasma cell leukemia. On the eighth hospital day, K. pneumoniae was identified in blood and sputum cultures. Fever improved after switching antibiotics, although his hematological condition worsened. His bone marrow cellularity (plasma cell proportion) progressively decreased: the values were 25% (80%), 10% (26%), 10% (11%), and < 10% (< 4%) on the 8th, 30th, 60th, and 90th hospital day, respectively. His plasmacytosis was extremely severe but was confirmed to be reactive with polyclonality. The present case represents the first report of strong suspicion of K. pneumoniae sepsis-associated marked plasmacytosis in an aplastic anemia patient.
Adult ; Anemia, Aplastic ; Anti-Bacterial Agents ; Biopsy ; Bone Marrow ; Fever ; Humans ; Klebsiella pneumoniae* ; Klebsiella* ; Leukemia, Plasma Cell ; Leukocyte Count ; Neutropenia ; Plasma ; Plasma Cells ; Pneumonia ; Sepsis ; Sputum ; Thrombocytopenia

PURPOSE: We investigated epidermal growth factor receptor(EGFR) expression in prostate cancer(PCa) and their potential role as predicting factor on biochemical recurrence(BCR). MATERIALS AND METHODS: Between February 2005 and February 2007, EGFR expression were prospectively evaluated in a consecutive series of 88 PCa patients with the following characteristics: 66 patients treated with retropubic radical prostatectomy(RRP); 22 patients treated with neoadjuvant hormonal therapy followed by RRP. The relationship between EGFR expression and several clinicopathologic parameters were evaluated. The probability of BCR-free survival was determined using the Kaplan-Meier method. RESULTS: EGFR expression, was evaluated by immunohistochemistry, was found in 31 of 88(35.2%) patients. 8 of 31 EGFR-positive patients(25.8%) had BCR, whereas only 5 of 57 EGFR-negative patients(8.8%) had BCR (p=0.031) during a median follow-up of 21 months. Among several variables, high serum prostate-specific antigen values(>or=20), extraprostatic extension, seminal vesicle invasion, and EGFR expression were the significant predictors of BCR on univariate analysis. But, multivariate analysis showed that no variable was significant predictor of BCR. EGFR-negative patients had a significantly longer mean BCR-free survival time than EGFR-positive patients(p=0.027). CONCLUSIONS: EGFR expression could be an potential predicting factor on BCR following RRP.

PURPOSE: The zygomatic arch is a key element which composes the facial contour. In many cases of zygomatic arch fracture, it is difficult to fix rigidly the fractured segments. If reduced bone segments were not fixed rigidly, they are proven to be displaced by mastication or unintentional external forces. So, unfixed zygomatic arch fracture after reduction may require a external device of prevention of collapse. We introduce a new protector which stabilizing the fractured segments to prevent for collapse of the reduced zygomatic arch fracture. METHODS: After reduction of zygomatic arch with blind approach(Gillies', Dingman or Keen's approach), bone segments was pulled with percutaneous traction suture in medial aspect of zygomatic arch. Then, the suture was fixed with Aqua splint(R), externally. And intraoperative and postoperative X-ray was done. The splint was removed on 14 days after the operation. RESULTS: 5 patients were treated with this method. 4 patients of total patients had no collapse in zygomatic arch. There was minimal collapse in one patient. Postoperative complications such as facial nerve injury, mouth opening difficulty, contour deformity, infection, scar were not observed. CONCLUSION: In comparison with other techniques, this technique has several advantages which are simple and easy method, short operation time, no scar, less soft tissue injury, and facilitated removal of splint. Therefore, Aqua splint(R) would be a good alternative to prevent for collapse in unstable zygomatic arch fractures
Cicatrix ; Congenital Abnormalities ; Facial Nerve Injuries ; Humans ; Mastication ; Mouth ; Postoperative Complications ; Soft Tissue Injuries ; Splints ; Sutures ; Traction ; Zygoma*

BACKGROUND AND OBJECTIVES: Bcl-2 protein is related to the inhibition of apoptosis via the mitochondrial pathway and Bcl-2's anti-oxidant effect. During the development of atherosclerosis, apoptosis is known to play an important role in the pathophysiologic behavior of atherosclerotic vascular disease in the medium-sized arteries. Apoptosis may be a compensatory reaction to regulate the cellular density of various tissues during the cellular proliferation process such as happens with tissue injury and during the development of atherosclerosis. The consequences of apoptosis in atherosclerosis may be related to the formation of an acellular lipid core, plaque instability and the loss of vascular wall integrity and remodeling. We sought to determine the effect of Bcl-2 gene expression on the development of primary atherosclerosis in apolipoprotein E deficient mouse, which is one of the typical animal models that are used for the development of peripheral atherosclerosis. MATERIALS AND METHODS: Bcl-2 transgenic mice were cross hybridized with apolipoprotein E deficient mice. Systemic analysis of the distribution and severity of their atherosclerotic lesions was done by dissecting microscopy, and the histological characteristics of the lesions were evaluated in normal chow-fed, 9-month-old apolipoprotein-E deficient/Bcl-2 transgenic mice (n=6) and apolipoprotein-E deficient mice (n=6). RESULTS: The distribution and severity of atherosclerotic lesions at the peripheral arteries were less in the apolipoprotein-E deficient/Bcl-2 transgenic mice. Acellular lipid core formation, destruction of the smooth muscle cell layers in the media and infiltration of inflammatory cells in the adventitia were much less in the apolipoprotein-E deficient/Bcl-2 transgenic mice. The lipid profile was similar in both groups. CONCLUSION: The effect of Bcl-2 gene expression on the peripheral atherosclerosis was related with the inhibition or the delay of atherosclerotic lesion progression, such as the reduction of amount of the acellular lipid core, maintenance of vascular smooth muscle cell integrity and the reduction of adventitial inflammation, and this was achieved regardless of serum cholesterol level.
Adventitia ; Animals ; Antioxidants ; Apolipoproteins* ; Apoptosis ; Arteries ; Atherosclerosis ; Cell Proliferation ; Cholesterol ; Genes, bcl-2* ; Humans* ; Infant ; Inflammation ; Mice* ; Mice, Transgenic ; Microscopy ; Models, Animal ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Vascular Diseases

BACKGROUND: To evaluate exudative pleural fluid, thoracentesis for microbiological and cytological examination and pleural biopsy by using a Cope needle are traditionally performed. Even after these studies, about 20% of patients remain undiagnosed. We evaluated the diagnostic accuracy and complications of 2-mm minithoracoscopy instead of blind biopsy in patients with undiagnosed exudative pleural effusion. METHOD: Fifteen patients with exudative pleural effusion underwent thoracoscopy between April 2002 and August 2003. The indication was undiagnosed pleural effusions after having performed sputum and pleural fluid examinations both microbiologically and cytologically. RESULT: The median age of the patients was 56 years (range 21-77). Pleural effusions were lymphocyte-dominant in 11 patients (73.3%) and neutrophil-dominant in 3 (20.0%). The remaining patient (6.7%) had pleural-fluid eosinophilia. Minithoracoscopic biopsy revealed accurate diagnosis in 14 patients (93.3%), consisting of tuberculous pleurisy in 8 (66.7%), malignant effusions in 4 (33.3%), and parapneumonic effusions in 2 (13.3%). One was diagnosed as having paragonimiasis from thoracoscopic findings and clinical considerations. There was no procedure-associated mortality. There were six cases of new onset fever (40%) and one of pneumothorax (6.7 %). CONCLUSION: Two-millimeter minithoracoscopy, which is less invasive than conventional thoracoscopy, was an accurate and safe method for undiagnosed exudative pleural effusion.
Biopsy* ; Diagnosis ; Eosinophilia ; Fever ; Humans ; Mortality ; Needles ; Paragonimiasis ; Pleural Effusion* ; Pneumothorax ; Sputum ; Thoracoscopy ; Tuberculosis, Pleural

BACKGROUND: CD43 is a sialoglycoprotein that is highly expressed on most leukocytes, except on B lymphocytes and dendritic cells. CD43 has been reported to be involved in the adhesion and apoptosis of lymphocytes. Although the aberrant expression of CD43 antigen in non-lymphoid tissues has been reported, the expression of the CD43 antigen in gastrointestinal malignancies is not well studied. Here, we studied the expression of CD43 in colon adenocarcinoma using the anti-CD43 monoclonal antibody developed in our laboratory. METHODS: Thirty patients who had undergone surgical resection for colorectal carcinoma were recruited. The expression of CD43 molecule was determined by analyzing the formalin-fixed, paraffin-embedded specimens immunohistochemically using our newly developed anti-CD43 mAb (K06). The results obtained by the immunohistochemical analysis correlated to the clinicopatho-logical parameters. RESULTS: The expression of CD43 were found in 20 out of 30 colorectal carcinoma cases. The expression of CD43 antigen is higher in well differentiated adenocarcinomas than poorly or moderately differentiated adenocarcinomas. CONCLUSIONS: The new anti-CD43 mAb might be helpful for the detection of the expression of CD43 on colorectal carcinoma cells. Further studies are required to assess the relationship between the CD43 expression and the colorectal carcinogenesis.
Adenocarcinoma ; Antigens, CD43 ; Apoptosis ; B-Lymphocytes ; Carcinogenesis ; Colon ; Colorectal Neoplasms ; Dendritic Cells ; Humans ; Immunohistochemistry ; Leukocytes ; Lymphocytes

Apoptotic cell death induced by p53 occurs at a late G1 cell cycle checkpoint termed the restriction(R)point, and it has been proposed that p53-induced apoptosis causes upregulation of CD95. However, as cells with defective in CD95 signaling pathway are still sensitive to p53-induced apoptosis, CD95 cannot be the sole factor resulting in apoptosis. In addition, unlike p53-induced apoptosis, the relationship between CD95-mediated apoptosis and the cell cycle is not clearly understood. It would there-fore be worth investigating whether CD95-mediated cell death is pertinent with p53-induced apoptosis in view of cell cycle related molecules. In this report, biochemical analysis showed that etoposide-induced apoptosis caused the induction and the nuclear translocation of effector molecules involved in G1 cell cycle checkpoint. However, there was no such translocation in the case of CD95-mediated death. Thus, although both types of apoptosis involved caspase activation, the cell cycle related proteins responded differently. This argues against the idea that p53-induced apoptosis occurs through the induction of CD95/CD95L expression.
Active Transport, Cell Nucleus ; Antigens, CD95/*metabolism ; *Apoptosis ; Cell Cycle ; Cell Nucleus/metabolism ; Coculture ; Dose-Response Relationship, Drug ; Down-Regulation ; Etoposide/pharmacology ; Flow Cytometry ; Human ; Immunoblotting ; Jurkat Cells ; Nucleic Acid Synthesis Inhibitors/pharmacology ; Protein Binding ; Protein Transport ; Protein p53/*metabolism ; Signal Transduction ; Up-Regulation