BACKGROUND: The apnea test is an essential component in the clinical determination of brain death, however it may incur a significant risk of complications such as hypotension, hypoxia and even cardiac arrest. We analyzed the risk factors associated with a failed apnea test during brain death assessment in order to predict and avoid these adverse events. METHODS: Medical records on apnea tests performed for brain-dead donors at our institution between January 2009 and January 2016 were retrospectively reviewed. Age, gender, etiology of brain death, use of catecholamines and results of arterial blood gas analysis (ABGA), systolic/diastolic blood pressure (SBP/DBP), mean arterial pressure and central venous pressure prior to apnea test initiation were collected as variables. A-a gradient and P(aO2)/F(iO2) were calculated for more precise assessment of the respiratory system. In total, 267 cases were divided into two groups based on those who completed the apnea test and those who failed the test. RESULTS: 13 cases failed the apnea test. Among them, seven cases failed due to severe hypotension (SBP < 60 mmHg) and the others failed due to refractory hypoxia. In terms of hemodynamic state, SBP was significantly higher in the completed test group than the failed group (126.5 ± 23.9 vs. 103 ± 15.2, respectively; p = 0.001). In ABGA, the completed test group showed significantly higher P(aO2)/F(iO2) (313.6 ± 229.8 vs. 141.5 ± 131.0, respectively; p = 0.008) and a lower A-a gradient (278.2 ± 209.5 vs. 506.2 ± 173.1, respectively; p = 0.000). In multivariable analysis, low SBP (p = 0.003) and high A-a gradient (p = 0.044) were independent risk factors associated with a failed apnea test. CONCLUSIONS: Although the unexpected adverse events during the apnea test for brain death determination do not occur frequently, they can be fatal. If a brain-dead patient has low SBP and a high A-a gradient, clinicians should pay more attention and prepare for potential complications prior to the apnea test.
Anoxia ; Apnea* ; Arterial Pressure ; Blood Gas Analysis ; Blood Pressure ; Brain Death* ; Brain* ; Catecholamines ; Causality ; Central Venous Pressure ; Heart Arrest ; Hemodynamics* ; Humans ; Hypotension ; Medical Records ; Respiratory System ; Retrospective Studies ; Risk Factors ; Tissue Donors

OBJECTIVE: To evaluate prospectively the efficacy and accuracy of transvaginal sonography(TVS), saline infusion sonohysterography(SIS) and hysteroscopy in the exploration of the uterine cavity. METHODS: 71 consecutive patients were evaluated with SIS who showed abnormal TVS findings, using saline instilled through endocervically placed balloon catheter with concurrent vaginal sonography. Among them, 41 patients also underwent hysteroscopy and surgery. Transvaginal sonography, sonohysterography, hysteroscopy were compaired with pathologic reports. RESULTS: Fifty-five of 71 sonohysterogram(77.5%) showed abnormal findings, Among them 41 patients have done hysteroscopy and biopsy. According to pathologic reports, sixteen patients were noted to have myoma(39.0%), twelve patients had polyps (21.3%), and both showed most frequent lesions. TVS, SIS, and hysteroscopy had a sensitivity of 94.4%, 91.1%, 94.4%, and a specificity of 40%, 42.8%, 60.0%, respectively and showed not so much different in detection rate. In case of submucosal myoma and polyps, hysteroscopy showed 100% sensitivity, and 92% specificity and showed much higher detection rate compared with SIS (81.2%, 92.0%). CONCLUSION: Transvaginal sonography and sonohysterography are good office diagnostic test in case of detecting variable gynecologic intrauterine abnormalities.
Biopsy ; Catheters ; Diagnostic Tests, Routine ; Humans ; Hysteroscopy* ; Myoma ; Polyps ; Prospective Studies ; Sensitivity and Specificity ; Uterine Hemorrhage*

No abstract available.
Extremities* ; Hyperplasia* ; Nevus*

No abstract available.
Deoxycholic Acid* ; Phosphatidylcholines* ; Prurigo*

BACKGROUND: Myocardial ischemia in human hypertension and in various animal models of hypertension may be due to abnormal maximal coronary vasodilator reserve and disturbaces of coronary vasomotion. The vascular reactivity defects in hypertension have been associated with the defective endothelium and sympathetic neural activation. However, such abnormalities in hypertension need to be elucidated. In the present study the effectsof cardiac ischemia reperfusion on coronary circulation, intramyocytic adenylates and purine nucleosides were examined in Langendorff-perfused Sprague Dawley rat (SD) and spontaneously hypertensive rat (SHR) hearts. Coronary venous and cardiac lactate and cardiac pyruvate were also measured. It should be noted that in the regulation of coronary flow the intrinsic flow autoregulation is highly variable due to coexisting metabolic flow control, and that natural coronary flow and cardiomyocytic energy state are normally reciprocally related in perfused heart. METHODS: For the Langendorff heart perfusion, bicarbonate perfusion buffer (pH 7.40+/-0.02,37degrees C) was equilibrated with 95% O2 : 5% CO2 and contained 5mM glucose (+5U/1 insulin) and 2mM pyruvate as energy-yielding substrates. Global hypoperfusion ischemia was induced by lowering coronary perfusion pressure of 100 to 40 cmH2O, followed by 20 min reperfusion. RESULTS: During the ischemia and reperfusion, metabolic acidosis and enhanced venous lactate output in SHR were observed with increases in coronary vascular resistance and myocardial oxygen consumption.In addition, coronary reactive hyperemia during reperfusion was depressed. Although ischemia-induced increase in combined adenosine plus inosine were abolished during prolonged reperfusion, SD still exhibited coronary vasodilation. The depressed reactive hyperemia in SHR was associated with decreases in cardiac adenosine triphosphate (ATP) pool and creatine phosphate/inorganic phosphate (CrP/Pi) ratio and an increase in cardiac lactate/pyruvate ratio. CONCLUSION: This abnormal vascular reactivity during ischemia and reperfusion in SHR may be in part due to an alteration in the cardiac energy state and hence to a mismatch between myocardial metabolic demand and supply.
Acidosis ; Adenosine ; Adenosine Triphosphate ; Animals ; Coronary Circulation ; Creatine ; Endothelium ; Glucose ; Heart* ; Homeostasis ; Humans ; Hyperemia ; Hypertension ; Inosine ; Ischemia ; Lactic Acid ; Models, Animal ; Myocardial Ischemia ; Oxygen ; Perfusion* ; Purine Nucleosides ; Pyruvic Acid ; Rats ; Rats, Inbred SHR* ; Reperfusion ; Vascular Resistance ; Vasodilation

No abstract available.
Breast Neoplasms* ; Breast* ; Eflornithine* ; Estrogens ; Humans* ; MCF-7 Cells ; Phosphorylation* ; Polyamines

No abstract available.
Diagnosis* ; Urinary Bladder Neoplasms* ; Urinary Bladder*

No abstract available.
Tooth Root ; Mandible ; Periodontal Ligament ; Bone Screws ; Dental Implantation

No abstract available.
Coronary Circulation* ; Heart* ; Rats, Inbred SHR*

BACKGROUNDS: Polyamines are known to be essential for cell growth and differentiation. Recently, possible roles of the polyamine in signal transduction as neurotransmitter, modulator, or second messenger are suggested in many studies. Furthermore, it is widely studied that possible roles of polyamine are involved in the action of hormone. Thus, it was to investigate the effect of polyamines in the cell proliferation and secretion of GH from the GH cells. METHODS: Cells(5*10 cells/mL) were incubated for 3 days in DMEM containing test drugs and labeled with 20pCi/mL of [S]-methionine for 2 hr. Proteins secreted into the medium were separated by 13% SDS-gel electrophoresis, then autoradiography was performed to identify radiolabeled proteins. [S]-methionine labelled GH was identified by radioimmuno-precipitation. Total protein synthesis was determined from the radioactivity of the cell homogenate by liquid scintillation counter. The intracellular polyamine content was determined by HPLC. RESULTS: Externally added polyamines(putrescine, spermidine, spermine) induced cell proliferation in a dose-dependent manner at proper concentrations, specifically 50pM putrescine increased GH secretion, DFMO or MGBG, which is polyamine biosynthetic inhibitor, inhibited GH secretion in a dose-dependent fashion, In the cells treated with 20mM or 0.01mM MGBG, total protein synthesis were decreased only to 90 or 76% of the control levels and cell proliferation was also slightly inhibited. However the secretion of GH was severely blocked to 37% or 35% of the control. Hydrocortisone at 5 pM stimulated the secretion of GH to 153% of basal secretion, also doubled intracellular putrescine content. CONCLUSION: The present data show that externally added polyamines induced cell proliferation and GH secretion. Also, extemally added putrescine stimulated GH secretion significantly. GH secretion was inhibited by polyamine metabolic inhibitor in a dose-dependent manner and polyamine metabolic inhibitors, at proper concentrations, specifically blocked GH secretion without any significant influence on the total protein synthesis. The above results imply the involvement of polyamine in GH secretion.
Autoradiography ; Cell Proliferation ; Chromatography, High Pressure Liquid ; Electrophoresis ; Growth Hormone ; Hydrocortisone ; Mitoguazone ; Neurotransmitter Agents ; Polyamines ; Putrescine ; Radioactivity ; Scintillation Counting ; Second Messenger Systems ; Signal Transduction ; Spermidine