No abstract available.
Echocardiography* ; Echocardiography, Doppler, Pulsed ; Heart Diseases* ; Heart*

No abstract available.
Heart Diseases* ; Heart*

No abstract available.
Arteries* ; Cardiomyopathy, Hypertrophic* ; Humans ; Infant* ; Mothers*

PURPOSE: The purpose of our study was to evaluate the volume of pre- and post operative masseter muscle and bite force in mandibular prognathic patients treated with SSRO with the use of the 3D CT imaging technique and occlusal force meter. MATERIALS AND METHODS: The study group consisted of 12 patients with mandibular prognathism (5 males and 7 females) who underwent mandibular setback surgery (BSSRO) in the Department of Oral and Maxillofacial Surgery, Samsung medical center. Bite force was measured at pre op, post op 3, 6 and 12 months by occlusal force meter(GM10, Nagano Keiki, Japan) The preoperative CT examination of subjects was performed between one month prior to operation and one year after to operation. And muscle volume was measured. RESULT: As compared to preoperative measurements at 1 year postoperatively the masseter and internal pterygoid muscle volume were diminished (p<0.05) The bite force steadily recovered, so at postoperatively 6 months reached the preoperative level. And at 1 year after operation, the maximum bite force was significantly greater than preoperative levels. No significant correlation was presented between masseter muscle and bite force (p>0.05), internal pterygoid muscle and bite force (p>0.05). CONCLUSION: In this study, the results showed that volume and bite force of the masticatory muscles decresed significantly immediate after orthognathic surgery for mandibular set-back. However, reduction of maximum bite force disappears within 6 months after surgery.
Bite Force ; Bites and Stings ; Humans ; Male ; Masseter Muscle ; Masticatory Muscles ; Muscles ; Orthognathic Surgery ; Prognathism ; Pterygoid Muscles ; Surgery, Oral

PURPOSE: Few reports have documented psychopathological abnormalities in patients with primary spontaneous pneumothorax (PSP). We analyzed the results of a multiphasic personal inventory test to investigate the psychopathologic impact of PSP in young Korean males. MATERIALS AND METHODS: The authors reviewed the results of a Korean military multiphasic personal inventory (KMPI) administered to military conscripts in South Korea. A total of 234 young males participated in this study. The normal volunteer group (n=175) comprised individuals who did not have any lung disease. The PSP group (n=59) included individuals with PSP. None of the examinees had any psychological problems. The KMPI results of both groups were compared. RESULTS: There were more abnormal responses in the PSP group (17.0%) than the normal volunteer group (9.1%, p=0.002). The anxiety scale and depression scale scores of the neurosis category were greater for the PSP group than the normal group (p=0.039 and 0.014, respectively). The personality disorder and paranoia scale scores of the psychopathy category were greater for the PSP group than the normal group (p=0.007 and 0.018, respectively). CONCLUSION: Young males with PSP may have greater tendencies to suffer from anxiety, depression, personality disorders, and paranoia compared to normal individuals. Clinicians should be advised to evaluate the psychopathological aspects of patients with PSP.
Anxiety ; Depression ; Healthy Volunteers ; Humans ; Korea ; Lung Diseases ; Male* ; Military Personnel ; Paranoid Disorders ; Personality Disorders ; Pneumothorax* ; Psychopathology

Leucine-rich repeat kinase 2 (LRRK2) is a gene that, upon mutation, causes autosomal-dominant familial Parkinson's disease (PD). Yeast two-hybrid screening revealed that Snapin, a SNAP-25 (synaptosomal-associated protein-25) interacting protein, interacts with LRRK2. An in vitro kinase assay exhibited that Snapin is phosphorylated by LRRK2. A glutathione-S-transferase (GST) pull-down assay showed that LRRK2 may interact with Snapin via its Ras-of-complex (ROC) and N-terminal domains, with no significant difference on interaction of Snapin with LRRK2 wild type (WT) or its pathogenic mutants. Further analysis by mutation study revealed that Threonine 117 of Snapin is one of the sites phosphorylated by LRRK2. Furthermore, a Snapin T117D phosphomimetic mutant decreased its interaction with SNAP-25 in the GST pull-down assay. SNAP-25 is a component of the SNARE (Soluble NSF Attachment protein REceptor) complex and is critical for the exocytosis of synaptic vesicles. Incubation of rat brain lysate with recombinant Snapin T117D, but not WT, protein caused decreased interaction of synaptotagmin with the SNARE complex based on a co-immunoprecipitation assay. We further found that LRRK2-dependent phosphorylation of Snapin in the hippocampal neurons resulted in a decrease in the number of readily releasable vesicles and the extent of exocytotic release. Combined, these data suggest that LRRK2 may regulate neurotransmitter release via control of Snapin function by inhibitory phosphorylation.
Amino Acid Sequence ; Animals ; Exocytosis ; Female ; HEK293 Cells ; Humans ; Mice ; Molecular Sequence Data ; Mutant Proteins/metabolism ; Phosphorylation ; Phosphothreonine/metabolism ; Protein Binding ; Protein Interaction Mapping ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*metabolism ; Qa-SNARE Proteins/metabolism ; Rats ; Rats, Sprague-Dawley ; Synaptosomal-Associated Protein 25/*metabolism ; Synaptotagmins/metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; Vesicular Transport Proteins/chemistry/*metabolism

PURPOSE: Non-steroidal anti-inflammatory drugs (NSAIDs) and statins are potential chemopreventive or chemotherapeutic agents. The mechanism underlying the deregulation of survivin by NSAIDs and statins in human non-small cell lung cancer cells has not been elucidated. In this study, we investigated the synergistic interaction of sulindac and simvastatin in lung cancer A549 cells. MATERIALS AND METHODS: Cell viability was measured by an MTT assay, while the expression of apoptotic markers, AKT, and survivin in response to sulindac and simvastatin was examined by Western blotting. DNA fragmentation by apoptosis was analyzed by flow cytometry in A549 cells. Reactive oxygen species (ROS) generation was measured by flow cytometry using H2DCFDA and MitoSOX Red, and the effects of pretreatment with N-acetylcysteine were tested. The effects of AKT on survivin expression in sulindac- and simvastatin-treated cells were assessed. Survivin was knocked down or overexpressed to determine its role in apoptosis induced by sulindac and simvastatin. RESULTS: Sulindac and simvastatin synergistically augmented apoptotic activity and intracellular ROS production in A549 cells. Inhibition of AKT by siRNA or LY294002 inhibited survivin, while AKT overexpression markedly increased survivin expression, even in the presence of sulindac and simvastatin. Moreover, survivin siRNA enhanced sulindac- and simvastatininduced apoptosis. In contrast, survivin upregulation protected against sulindac- and simvastatin-induced apoptosis. CONCLUSION: Combined treatment with sulindac and simvastatin augmented their apoptotic potential in lung cancer cells through AKT signaling-dependent downregulation of survivin. These results indicate that sulindac and simvastatin may be clinically promising therapies for the prevention of lung cancer.
Acetylcysteine ; Anti-Inflammatory Agents, Non-Steroidal ; Apoptosis* ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung ; Cell Survival ; DNA Fragmentation ; Down-Regulation* ; Flow Cytometry ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lung Neoplasms* ; Oncogene Protein v-akt ; Reactive Oxygen Species ; RNA, Small Interfering ; Simvastatin* ; Sulindac* ; Up-Regulation

PURPOSE: Gynecomastia is a common male breast abnormality and primarily occurs in puberty and senescence. The obvious etiological role of hormonal changes in gynecomastia, plus the discovery of estrogen receptor in normal and neoplastic breast, has spurred several investigations of ER content in male gynecomastic tissues. The results have been inconsistent and the fraction of ER-positive specimens has varied from 0~90%. METHODS: Immunohistochemical hormonal receptor analysis using monoclonal estrogen receptor (ER) alpha, beta and progesteron receptor (PR) was performed on the breast tissues of 58 patients with gynecomastia between January 1995 and January 2000 in the Department of Surgery, Uijongbu St. Mary's Hospital. These results were statistically compared with clinical data. RESULTS: 48 cases (82.8%) were ERalpha positive and 55 cases (94.8%) were ERbeta positive and PR positivity was noted in 55 cases (94.8%). There was negative relationship between ERalpha and age, PR and location. CONCLUSION: This study demonstrates that intracellular steroid receptors are present in most gynecomastic tissues. Additionally, it supports the general assumption that estrogen and progesteron may be two of the hormones responsible for the development of gynecomastia.
Male ; Humans

Human cytomegalovirus (CMV) infection has been a major concern in hematopoietic stem cell transplant recipients. Ganciclovir (GCV) resistance results mostly from mutations within the protein kinase UL97 gene. The three hot spots for GCV resistance (codons 460, 520, and 590-607) were well known. We describe a case of GCV-resistant CMV colitis caused by a 597-600 deletion in UL97 after haplo-identical peripheral blood stem cell transplantation (h-PBSCT) in a 46 year-old man with myelodysplastic syndrome. On post-PBSCT day 28, CMV antigenemia turned positive. Treatment of GCV was started and continued for 12 weeks but CMV antigenemia did not respond to the treatment and CMV colitis was worsened. The UL97 showed the in-frame deletion between codons 597 and 600 by direct sequencing. The treatment was switched to foscarnet and the antigenemia test was consecutively negative twice, and clinical symptoms improved. Despite the recovery of the patient from CMV colitis, the patient expired post-PBSCT day 146 from acute liver failure, hepatorenal syndrome and septic shock. This case is a first report of a deletion 597-600 in CMV UL97 in Korea. A 597-600 deletion in UL97 was responsible for the GCV resistance while preserving susceptibility to foscarnet.
Codon ; Colitis* ; Cytomegalovirus* ; Drug Resistance ; Foscarnet ; Ganciclovir ; Hematopoietic Stem Cells ; Hepatorenal Syndrome ; Humans ; Korea ; Liver Failure, Acute ; Myelodysplastic Syndromes ; Peripheral Blood Stem Cell Transplantation ; Protein Kinases ; Shock, Septic ; Stem Cell Transplantation* ; Transplantation

PURPOSE: In order to confirm the clinical application of a tissue microarrays method, the expression rate and relationship between factors related apoptosis, hormonal receptors and the clinical factors were investigated. METHODS: A tissue microarrays of 59 breast cancer tissues, and apoptosis related factors were examined by immunohistochemical staining using monoclonal antibodies. RESULTS: The median age of the patients was 49.9 years and 86.4% had a pathological stage of over stage II. The average number of metastatic lymph nodes was 3.8. p53 expression was noted in 21 cases (35.6%) and was related to Bcl-2, ER and PR expression. PTEN was expressed in 39 cases (66.1%) and related to FAS, Bcl-2, ER and PR expression. Fas was expressed in 34 cases (57.6%) and related with PR and BAX expression. BAX expression was observed in 42 cases (71.2%) and was related to the metastatic axillary lymph nodes, and both Bcl-2 and PR expression. Bcl-2 expression was noted in 33 cases (55.9%) and related to ER and PR expression. ER was expressed in 34 cases (57.6%) and was related positively with PR expression. CONCLUSION: The tissue microarrays method can be used for both screening and analyzing many factors or different tumor types. This new technique may be very powerful for the rapid identification of the tumor characteristics.
Antibodies, Monoclonal ; Apoptosis* ; Breast Neoplasms* ; Breast* ; Humans ; Lymph Nodes ; Mass Screening