Hypercalcemia is one of the most common paraneoplastic syndromes and believed to occur through two general mechanisms, one humoral and the other local. The former mechanism has been termed humoral hypercalcemia of malignancy (HHM) and has been associated with the secretion of various cytokines, including parathyroid hormone-related protein (PTHrP). PTHrP beats sttuctural and functional similarities to PTH and seems to play a key role in the pathogenesis of HHM. We experienced the case of HHM associated with hepatoma, a rare cause of HHM, in 48 year-old male. We found no evidence of bone metastasis. In this case, contrary to our general acknowledgment, serum 1,25 (OH)D concentration was elevated. We report this case with a brief review of related literatures.
Carcinoma, Hepatocellular* ; Cytokines ; Humans ; Hypercalcemia* ; Male ; Middle Aged ; Neoplasm Metastasis ; Paraneoplastic Syndromes ; Parathyroid Hormone-Related Protein*

Jugular bulb diverticulum (JBD) is a rarely reported vascular anomaly, which is an extraluminal outpouching from the jugular bulb. Especially, there exists a lack of reported cases involving JBD encroaching the internal auditory canal (IAC) in Korea. Subjects with JBD may be asymptomatic or have variable symptoms based on its location and size. In this article, we report a unique case of JBD eroding into the IAC that was presented as sudden sensorineural hearing loss with vertigo.
Cytochrome P-450 CYP1A1 ; Diverticulum ; Hearing Loss ; Hearing Loss, Sensorineural ; Korea ; Vertigo

BACKGROUND: In the present study, we examined the effect of morphine on NO- and peroxynitrite-induced cell death using a human neuroblastoma SH-SY5Y cell line which abundantly expresses micro, delta and K-opioid receptors. METHODS: The cultured cells were pretreated with morphine (100 micrometer) and exposed to 3-morpholinosydnonimine (SIN-1, 1mM). Agarose gel electrophoresis of DNA was done with the extracts from SH-SY5Y cells. The cells were treated with selective ligands for opioid receptor subtypes and with PI3-kinase inhibitors. Cell damage was assessed by using an MTT assay. Spectrophotometric absorption spectra were measured from the mixture of morphine (100 micrometer) plus peroxynitrite (1 mM) at room temperature. RESULTS: SIN-1 treated cells showed the occurrence of a specific form of chromosomal DNA fragmentation which pretreatment with morphine inhibited. The selective ligands for opioid receptor subtypes, [D-Ala2, N-Me-Phe4, Gly-ol5]enkephalin (DAMGO, micro-opioid receptor agonist), [D-Pen2,5] enkephalin (DPDPE, delta-opioid receptor agonist) and U-69593 (K-opioid receptor agonist) at a concentration of 10 micrometer did not prevent the cell death induced by SIN-1. Naloxone (20 micrometer) hardly antagonized the effect of morphine in SIN-1-induced cell death. The PI3-kinase inhibitors Wortmannin and LY294002 did not inhibit the action of morphine on apoptotic cell death. In the measurements of spectrophotometric absorption spectra, the peak of the absorbance of the mixture of morphine plus peroxynitrite at 295 300 nm disappeared three minutes after mixing. CONCLUSIONS: The present study showed that morphine protected the human neuroblastoma cell line,SH-SY5Y, from peroxynitrite-induced apoptotic cell death. However, it is suggested that the protective action of morphine is not via the activation of opioid receptors and/or the PI3-kinase pathway but possibly via direct chemical reaction.
Absorption ; Cell Death ; Cell Line ; Cells, Cultured ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Enkephalins ; Humans* ; Ligands ; Morphine* ; Naloxone ; Neuroblastoma* ; Peroxynitrous Acid ; Phosphatidylinositol 3-Kinases ; Receptors, Opioid

BACKGROUND: Antihypertensive agents such as verapamil and esmolol are well known for their effects of hemodynamic stabilization on tracheal intubation. However, our previous study, Verapamil and esmolol did not attenuate heart rate and blood pressure. The aim of the present study was to evaluate the efficacy of combined administration of these drugs for controlling hemodynamic responses to tracheal intubation. METHODS: Forty-eight patients, ASA physical status I or II, were randomly assigned to one of four groups (n = 12 each):normal saline (control), verapamil 0.1 mg/kg, esmolol 1 mg/kg, and verapamil 0.05 mg/kg mixed with esmolol 0.5 mg/kg. Anesthesia was induced with thiopental 5 mg/kg intravenously, and then saline, verapamil, esmolol or the mixed drugs were administered as an intravenous bolus, and immediately followed by succinylcholine 1.5 mg/kg. Tracheal intubation was performed 90 s after intravenous injection of experimental drugs. Systolic and diastolic blood pressure and heart rate were measured before induction and every minute for 5 minutes after tracheal intubation. RESULTS: There was a significant attenuation in systolic blood pressure after tracheal intubation in the verapamil and mixed groups compared to the control and esmolol groups. Heart rates were significantly lower in the esmolol and mixed groups than in the verapamil groups after tracheal intubation. CONCLUSIONS: Combined administration of Verapamil 0.05 mg/kg with esmolol 0.5 mg/kg attenuated increases in blood pressure and heart rate after tracheal intubation.
Anesthesia ; Antihypertensive Agents ; Blood Pressure* ; Heart Rate* ; Heart* ; Hemodynamics ; Humans ; Injections, Intravenous ; Intubation* ; Succinylcholine ; Thiopental ; Verapamil*

BACKGROUND: Antihypertensive agents such as verapamil and esmolol are well known for their effects of hemodynamic stabilization on tracheal intubation. But hemodynamic discrepancies in these agents may result from different techniques of anesthetic induction. The aim of the present study was to compare and evaluate their efficacy in controlling hemodynamic responses to tracheal intubation under the different anesthetic induction agents. METHODS: Seventy-two patients, ASA physical status I or II, were randomly assigned to one of six groups (n = 12 each): a Thiopental-Saline (T-S) group and a Propofol-Saline (P-S) group in saline 10 ml; a Thiopental-Verapamil (T-V) group and a Propofol-Verapamil (P-V) group in verapamil 0.1 mg/kg; a Thiopental-Esmolol (T-E) group and a Propofol-Esmolol (P-E) group in esmolol 1 mg/kg according to the induction agents, thiopental or propofol. Anesthesia was induced with thiopental 5 mg/kg or propofol 2 mg/kg intravenous, respectively. Next, saline, verapamil and esmolol were administered as a bolus, and were immediately followed by succinylcholine 1.5 mg/kg. Tracheal intubation was carried out 60 s and 90 s after the intravenous injections of verapamil and esmolol, respectively. Systolic and diastolic blood pressure and heart rate were measured before induction and every minute for 5 minutes after tracheal intubation. RESULTS: There was a significant attenuation in systolic and diastolic arterial pressure after tracheal intubation in the verapamil groups compared to the esmolol groups. Heart rates were significantly lower in the esmolol groups than in the verapamil groups after tracheal intubation. CONCLUSIONS: Verapamil 0.1 mg/kg and esmolol 1 mg/kg attenuated increases in blood pressure and heart rate after tracheal intubation. The different anesthetic induction agents did not influence the hemodynamic effects of verapamil and esmolol on tracheal intubation.
Anesthesia ; Antihypertensive Agents ; Arterial Pressure ; Blood Pressure* ; Heart Rate* ; Heart* ; Hemodynamics ; Humans ; Injections, Intravenous ; Intubation* ; Propofol ; Succinylcholine ; Thiopental ; Verapamil*

BACKGROUND: Antihypertensive agents such as verapamil and esmolol are well known for their effects of hemodynamic stabilization on tracheal intubation. But hemodynamic discrepancies in these agents may result from different techniques of anesthetic induction. The aim of the present study was to compare and evaluate their efficacy in controlling hemodynamic responses to tracheal intubation under the different anesthetic induction agents. METHODS: Seventy-two patients, ASA physical status I or II, were randomly assigned to one of six groups (n = 12 each): a Thiopental-Saline (T-S) group and a Propofol-Saline (P-S) group in saline 10 ml; a Thiopental-Verapamil (T-V) group and a Propofol-Verapamil (P-V) group in verapamil 0.1 mg/kg; a Thiopental-Esmolol (T-E) group and a Propofol-Esmolol (P-E) group in esmolol 1 mg/kg according to the induction agents, thiopental or propofol. Anesthesia was induced with thiopental 5 mg/kg or propofol 2 mg/kg intravenous, respectively. Next, saline, verapamil and esmolol were administered as a bolus, and were immediately followed by succinylcholine 1.5 mg/kg. Tracheal intubation was carried out 60 s and 90 s after the intravenous injections of verapamil and esmolol, respectively. Systolic and diastolic blood pressure and heart rate were measured before induction and every minute for 5 minutes after tracheal intubation. RESULTS: There was a significant attenuation in systolic and diastolic arterial pressure after tracheal intubation in the verapamil groups compared to the esmolol groups. Heart rates were significantly lower in the esmolol groups than in the verapamil groups after tracheal intubation. CONCLUSIONS: Verapamil 0.1 mg/kg and esmolol 1 mg/kg attenuated increases in blood pressure and heart rate after tracheal intubation. The different anesthetic induction agents did not influence the hemodynamic effects of verapamil and esmolol on tracheal intubation.
Anesthesia ; Antihypertensive Agents ; Arterial Pressure ; Blood Pressure* ; Heart Rate* ; Heart* ; Hemodynamics ; Humans ; Injections, Intravenous ; Intubation* ; Propofol ; Succinylcholine ; Thiopental ; Verapamil*

No abstract available.
Female* ; Humans ; Neck* ; Urinary Bladder* ; Urinary Incontinence*

No abstract available.
Vulva*

BACKGROUND: The effect of opioids on nitric oxide (NO)- and peroxynitrite-induced neuronal cell death is largely unknown. In the present study, we examined the effect of morphine on NO- and peroxynitrite-induced cell death using a human neuroblastoma SH-SY5Y cell line, which abundantly expresses micro, delta, kappa-opioid receptors. METHODS: The cultured cells were pretreated with morphine and exposed to 3-morpholinosydnonimine (SIN-1) that simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using MTT assay and crystal violet staining. Morphological nuclear changes and enzymatic evidences of apoptosis of the cells after exposure to SIN-1 for 24 hours were evaluated by using 4', 6-diamidino-2-phenylindole (DAPI) staining and the measurement of pro-apoptotic protease (caspase-3) activity, respectively. Levels of reduced glutathion (GSH) were measured by monochloronimane (MCB) assay. RESULTS: Pretreatment of SH-SY5Y with morphine significantly inhibited the apoptotic cell death. Morphine also inhibited SIN-1-induced caspase-3 (pro-apoptotic protease) activity in a dose-dependent manner. However, naloxone (20 microM) could not antagonize completely the effect of morphine in SIN- 1-induced cell death. Pre-administered GSH and N-acetylcysteine (NAC) have been found to protect SIN-induced apoptosis, and the neuroblastoma cells treated with morphine had significantly elevated the levels of GSH. CONCLUSIONS: The present study shows that morphine protects the human neuroblastoma cell line SH- SY5Y from peroxynitrite-induced apoptotic cell death through elevated GSH levels. The protective actionof morphine seems to be associated with inhibition of the apoptotic pathway. However, it is suggested that morphine protects the cells possibly via other unknown mechanisms in addition to the activation of opioid receptors.
Acetylcysteine ; Analgesics, Opioid ; Apoptosis* ; Caspase 3 ; Cell Death ; Cell Line ; Cells, Cultured ; Gentian Violet ; Humans* ; Morphine* ; Naloxone ; Neuroblastoma* ; Neurons ; Nitric Oxide ; Peroxynitrous Acid ; Receptors, Opioid ; Superoxides

Proteasomes are the primary degradation machinery for oxidatively damaged proteins that compose a class of misfolded protein substrates. Cellular levels of reactive oxygen species increase with age and this cellular propensity is particularly harmful when combined with the age-associated development of various human disorders including cancer, neurodegenerative disease and muscle atrophy. Proteasome activity is reportedly downregulated in these disease conditions. Herein, we report that docosahexaenoic acid (DHA), a major dietary omega-3 polyunsaturated fatty acid, mediates intermolecular protein cross-linkages through oxidation, and the resulting protein aggregates potently reduce proteasomal activity both in vitro and in cultured cells. Cellular models overexpressing aggregation-prone proteins such as tau showed significantly elevated levels of tau aggregates and total ubiquitin conjugates in the presence of DHA, thereby reflecting suppressed proteasome activity. Strong synergetic cytotoxicity was observed when the cells overexpressing tau were simultaneously treated with DHA. Antioxidant N-acetyl cysteine significantly desensitized the cells to DHA-induced oxidative stress. DHA significantly delayed the proteasomal degradation of muscle proteins in a cellular atrophy model. Thus, the results of our study identified DHA as a potent inducer of cellular protein aggregates that inhibit proteasome activity and potentially delay systemic muscle protein degradation in certain pathologic conditions.
Atrophy ; Cells, Cultured ; Cysteine ; Humans ; In Vitro Techniques* ; Muscle Fibers, Skeletal* ; Muscle Proteins ; Muscular Atrophy* ; Neurodegenerative Diseases ; Oxidative Stress ; Proteasome Endopeptidase Complex* ; Protein Aggregates* ; Reactive Oxygen Species ; Ubiquitin