It has been clarified that myoepithelial cells contain S-100 protein which is known to be a marker protein of neural tissue. To evaluate the participation of myoepithelial cells in the histogenesis of the salivary gland tumors, normal salivary glands and various salivary gland tumors were stained by immuno-peroxidase method. PAP kits (DAKO Co, USA) for the S-100 protein and the Cytokeratin were used and the following resulting were obtained. Acinic cells of the normal salivery gland were negative for both cytokeratin and S-100 protein. The intercalated duct cells were weakly positive for cytokeratin and S-100 protein. The normal myoepithelial cells scattered around the acini and the intercalated ducts were positive only S-100 protein. In contrast, the striated duct were positive only for cytokeratin. In plemorphic adenoma, the S-100 protein positive cells were found in solid sheets of tumor cells, in chondromyxoid areas and in areas of spindle-cell stroma as well as in the outer layer of the tubular structures. Only the inner lining of the tubules were positive for cytokeratin. In basal cell adenoma, the stromal spindle cells were strongly positive for S-100 protein and the epithelial cells weakly positive. When tubules were present within the epithelial sheets, the inner most lining cells were positive for cytokeratin. The peripheral palisaded tumor cells were negative for both substances. By immunostaining of the adenoid cystic carcinoma, S-100 protein containing cells were found focally scattered independently on the variety of histologies. The lining cells of true cystic structure were positive for cytokeratin. Immunostaining of the mucoepidermoid carcinoma demostrated that the squamous cells and the tubular epithelial cells contained cytokeraitn, whereas only a few intermediate cells were positive for S-100 protein. In Warthin's tumor there were no S-100 protein positive cells, although basally located epithelial cells of the papillae were positive for cytokeratin. These findings suggest that salivary gland tumors other than the Warthin's tumor arise from myoepithelial cells or reserve cells having dual potentiality differentating into myoepithelial and intercalcated duct cells.

BACKGROUND: ST segment elevation in patient with chest pain was seen in acute myocardial infarction and in numerous other non-infarction syndrome. The causes of non-infarction syndrome were left ventricular hypertrophy, BER(benign early repolarization), and left bundle branch block in cardiac origin and were hyperkalemia and hyperventilation syndrome in metabolic origin and were others. Furthermore, the differentiation of electrocardiogram between acute myocardial infarction and non-infarction syndrome was very difficult. So, we compared and analysed characteristics of ST segment elevation of acute myocardial infarction and non-infarction syndrome that suggested the clue of early diagnosis of coronary artery disease. METHOD AND MATERIALS: We retrospectively reviewed the electrocardiogram of 961 patients with chest pain who visited the emergency center from January 1999 to December 1999. Acute myocardial infarction was diagnosed by clinical finding, electrocardiogram, cardiac enzyme, echocardiogram, and myocardial spect. Left ventricular hypertrophy, BER, and left bundle branch block in cardiac origin of non-infarction syndrome were diagnosed by electrocardiographic criteria suggested by William J. Brady. Acute myocarditis, acute pericarditis, and hyperventilation syndrome were diagnosed by clinical finding. RESULTS: Among 961 patients with chest pain, 236(24.6%) patients manifested ST segment elevation who were diagnosed acute myocardial infarction in 162(68.6%) patients and non-infarction syndrome in 74(31.4%) patients. The causes of non-infarction syndrome in 74 patients were left ventricular hypertrophy(32:13.6%), BER(28:11.9%), left bundle branch block(11:4.7%), and others(3:1.3%). Three others were acute myocarditis, acute pericarditis, and hyperventilation syndrome. Electrocardiographic characteristics of ST segment elevation of non-infarction syndrome manifested almost same finding compared to William J. Brady' criteria. CONCLUSION: ST segment elevation in patient with chest with chest pain visited emergency department was seen in acute myocardial infarction(68.6%) and the other non-infarction syndromes(31.4%). Significant number of patients were not associated with acute myocardial infarction. Therefore, we must completely understand characteristics of ST segment elevation in acute myocardial infarction and the other non-infarction syndromes to diagnose fatal early coronary artery disease and to avoid unnecessary thrombolytic therapy.
Bundle-Branch Block ; Chest Pain* ; Coronary Artery Disease ; Early Diagnosis ; Electrocardiography ; Emergencies ; Emergency Service, Hospital ; Humans ; Hyperkalemia ; Hypertrophy, Left Ventricular ; Hyperventilation ; Myocardial Infarction* ; Myocarditis ; Pericarditis ; Retrospective Studies ; Thorax* ; Thrombolytic Therapy ; Tomography, Emission-Computed, Single-Photon

No abstract available.
Nevus*

No abstract available.
Dermoid Cyst*

Ischemic brain hippocampal formation has been developed to understand the relationship between delayed neuronal damage and the expression of NMDA receptor subunits[NR2A, NR2B], MAP2, and NF200 in ttle conditions of hypoxia. Changes of NR subunits[NR2A, 2B], MAP2 6nd NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by morphological change, cytoskeletal disruption was examined through H & E, toluidine blue and immunohistochemical studies. The expression of NR2B was increased than normal at 30 hours after hypoxia. At this time, the expression of MAP2 and NF200 was markedly decreased and their morphology was more eosinophilic than normal and then became darker with expanded perineuronal space. Irreversible neuronal cell damage in hypoxic hippocampal formation is most prominent in CA3 region of hippocampus and the process is triggered by Ca2+ influx through NR1/MR2B receptor channel at 30 hour after initial hypoxic insult. Ca2+ influx through NR1/MR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which causes neuronal cell death. And, morphological changes of neuronal cells in hypoxic conditions were manifested as red neurons in the stage of reactive change, and as dark neuron in the stage of late hypoxic cell damage.
Animals ; Anoxia* ; Brain ; Cell Death ; Cell Membrane ; Cytoskeleton ; Eosinophils ; Hippocampus* ; N-Methylaspartate ; Neurons ; Peptide Hydrolases ; Proteolysis ; Rats* ; Receptors, N-Methyl-D-Aspartate ; Tolonium Chloride

Bilateral diaphragmatic paralysis(BDP) is a rare disorder, which can be secondary to spinal cord injury, motor neuron disease, myopathy, noninfectious polyneuropathy, infection, iced saline cardioplegia performed during cardiac surgery, or idiopathic causes. there may be typical presentations such as dyspnea, paradoxical respiratory movement, and hypercapnic respiratory failure. It needs to exclude above secondary causes to consider idiopathic bilateral diaphragmatic paralysis. We report a 51-years-old man who presented with idiopathic bilateral diaphragmatic paralysis combined with acute pancreatitis. We couldnt, find out the association of these two clinical conditions. The patient was improved by mechanical ventilation.
Dyspnea ; Heart Arrest, Induced ; Humans ; Motor Neuron Disease ; Muscular Diseases ; Pancreatitis* ; Polyneuropathies ; Respiration, Artificial ; Respiratory Insufficiency ; Respiratory Paralysis* ; Spinal Cord Injuries ; Thoracic Surgery

BACKGROUND: More than 90% of acute stroke patients have measurable cardiovascular sequelae, but we have been often overlooked in formal discussions of treatment. If we estimate the incidence of myocardial injury in patient with spontaneous SAH, we may figure the possibility of cardiac dysfunction in such patients. This study was designed to investigate the incidence of myocardial injury in patients with spontaneous SAH using cardiac troponin I(cTnI). METHODS: A prospective single emergency center study was performed to determined preoperative incidence of unrecognized cardiac injury in patients suffering spontaneous SAH. We include the spontaneous SAH patients who underwent serum measurements of the cardic troponin I immediately upon admission last six month period. ECG, CK, CK-MB and myoglobin were also performed at admission. We excluded the spontaneous SAH patients who had past history of myocardial ischemia and ECG abnormality. RESULTS: Fifty-two patients(34 females, 18 males) with spontaneous SAH were studied prospectively. 18 patients(34.6% of the total study population) had cTnI level above 0.5ng/ml. ECG was performed in 52 patients and was abnormal in 15 of the 52 patients(28.8%). CONCLUSION: The measurement of cTnI has provided physicians with a myocardial marker that has a cardiac sensitivity for cardiac injury equal to that of CK-MB yet with greater specificity. So, cardiac troponin I is useful to estimate the incidence of myocardial injury in patients with spontaneous SAH. And we may estimate the possibility of cardiac dysfunction in such patients. This knowledge will hopefully aid in the care and improve the outcome.
Electrocardiography ; Emergencies ; Female ; Humans ; Incidence* ; Myocardial Ischemia ; Myoglobin ; Prospective Studies ; Sensitivity and Specificity ; Stroke ; Troponin I* ; Troponin*

No abstract available.
Lasers, Dye* ; Melanosis*

As the number of young cancer survivors increases, quality of life after cancer treatment is becoming an ever more important consideration. According to a report from the American Cancer Society, approximately 810,170 women were diagnosed with cancer in 2015 in the United States. Among female cancer survivors, 1 in 250 are of reproductive age. Anticancer therapies can result in infertility or sterility and can have long-term negative effects on bone health, cardiovascular health as a result of reproductive endocrine function. Fertility preservation has been identified by many young patients diagnosed with cancer as second only to survival in terms of importance. The development of fertility preservation technologies aims to help patients diagnosed with cancer to preserve or protect their fertility prior to exposure to chemo- or radiation therapy, thus improving their chances of having a family and enhancing their quality of life as a cancer survivor. Currently, sperm, egg, and embryo banking are standard of care for preserving fertility for reproductive-age cancer patients; ovarian tissue cryopreservation is still considered experimental. Adoption and surrogate may also need to be considered. All patients should receive information about the fertility risks associated with their cancer treatment and the fertility preservation options available in a timely manner, whether or not they decide to ultimately pursue fertility preservation. Because of the ever expanding number of options for treating cancer and preserving fertility, there is now an opportunity to take a precision medicine approach to informing patients about the fertility risks associated with their cancer treatment and the fertility preservation options that are available to them.
Adult Stem Cells ; Cell Culture Techniques ; Cryopreservation/*methods ; *Embryo, Mammalian ; Female ; Fertility Preservation/*methods ; Humans ; Neoplasms/drug therapy/*therapy ; *Oocytes ; Ovarian Follicle/drug effects/metabolism/transplantation ; *Ovary/transplantation ; Ovulation Induction/methods ; Precision Medicine

No abstract available.
Female ; Humans ; *Ovary ; *Uterus