The antimicrobial agents reduced infectious diseases significantly. However, antibiotic resistance has followed for almost every antimicrobial agent. Especially, Staphylococcus aureus was one of the most notorious for the multidrug resistance. Streptomyces sp. 681 has been selected for antibiotic-producing strain against methicillin-resistant Staphylococcus aureus (MRSA) from 1,000 strains of Actinomycetales which had been isolated from soil. In antimicrobial susceptibility test, all of the test strains were susceptible to vancomycin. However, most strains of Staphylococcus aureus were found to be resistant to methicillin. Ninety eight (75%) strains out of 129 strains showed multiple resistance pattern to more than 5 antimicrobial agents. The MIC values of the purified antibiotic (K-681) were 1-32 ug/ml against Gram-positive bacteria compared to >128 ug/ml against Grarn-negative bacteria or fungi. The MIC was 8 ug/ml for 90% of the 129 clinical isolates of S. aureus. The antibiotic showed no cytotoxicity against P 388, HeLa, and S180 at the concentration of 500 ug/ml.
Actinomycetales ; Anti-Infective Agents ; Bacteria ; Communicable Diseases ; Drug Resistance, Microbial ; Drug Resistance, Multiple ; Fungi ; Gram-Positive Bacteria ; Methicillin ; Methicillin-Resistant Staphylococcus aureus ; Soil ; Staphylococcus aureus* ; Staphylococcus* ; Streptomyces* ; Vancomycin

No abstract available
Hemodynamics*

Pioglitazone (PGZ), a synthetic peroxisome proliferator-activated receptor gamma agonist, is known to regulate inflammatory process and to have neuroprotective effects against neurological disorders. In the present study, we examined the effects of 30 mg/kg PGZ on excitotoxic neuronal damage and glial activation in the mouse hippocampus following intracerebroventricular injection of kainic acid (KA). PGZ treatment significantly reduced seizure-like behavior. PGZ had the neuroprotective effect against KA-induced neuronal damage and attenuated the activations of astrocytes and microglia in the hippocampal CA3 region. In addition, MPO and NFkappaB immunoreactivities in the glial cells were also decreased in the PGZ-treated group. These results indicate that PGZ had anticonvulsant and neuroprotective effects against KA-induced excitotocix injury, and that neuroprotective effect of PGZ might be due to the attenuation of KA-induced activation in astrocytes and microglia as well as KA-induced increases in MPO and NFkappaB.
Animals ; Astrocytes ; CA3 Region, Hippocampal ; Hippocampus* ; Kainic Acid ; Mice* ; Microglia ; Nervous System Diseases ; Neuroglia ; Neurons* ; Neuroprotective Agents ; PPAR gamma

Testicular granulosa cell tumor(GCT) is a rare neoplasm. We report here on an incidentally discovered testicular granulosa cell tumor in a 36-year-old man. The serum tumor markers were within the normal limits. The ultrasonographic findings revealed a mass with a heterogenous hypoechoic echotexture, including multiple variable sized cystic components. The histology on the orchiectomy specimen demonstrated a gonadal stromal tumor with granulosa cell features. Testicular granulosa cell tumor of the adult type is a very rare tumor, and there have been several isolated case reports and small serial studies described in the literature.
Adult ; Female ; Gonads ; Granulosa Cell Tumor ; Granulosa Cells ; Humans ; Orchiectomy ; Testicular Neoplasms ; Testis ; Biomarkers, Tumor

BACKGROUND: Sevoflurane is the most recently available volatile agent which permits the rapid induction with its nonirritant nature. The goal of this study was to compare the hemodynamic responses of sevoflurane induction and maintenance period with those of fentanyl-midazolam/isoflurane anesthesia for CABG. METHODS: Twenty-eight patients who underwent CABG were given anesthesia, and were randomly assigned to receive sevoflurane (Sevo Group, n = 15) or fentanyl-midazolam/isoflurane (Iso-Fent Group, n = 13), as induction and maintenance agents. In the Sevo group, anesthesia was induced with two or three deep breaths of 7.5% sevoflurane, and maintained with 2% sevoflurane after intubation. The Iso-Fent Group received fentanyl 5microgram/kg and midazolam 0.2 mg/kg with oxygen for induction and maintained with 0.8% isoflurane and 5microgram/kg/hr of fentanyl by infusion. All were given vecuronium as a muscle relaxant. Cardiac and oxygen metabolic profiles were measured before and 10 minutes after tracheal intubation. RESULTS: Before induction, there was no difference between Sevo and Iso-Fent group in terms of cardiac and oxygen metabolic profiles. After intubation, mean arterial pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, heart rate and mixed venous oxygen saturation in the Sevo group were higher than in the Iso-Fent group (P < 0.05). The ST-segment changes in the EKG monitoring was unremarkable during anesthesia induction in either group. CONCLUSIONS: For the induction and early anesthesia maintenance in patients undergoing CABG surgery, sevoflurane may be a substitute for fentanyl-midazolam/isoflurane without any significant hemodynamic changes.
Anesthesia* ; Arterial Pressure ; Coronary Artery Bypass* ; Coronary Vessels* ; Electrocardiography ; Fentanyl ; Heart Rate ; Hemodynamics* ; Humans ; Intubation ; Isoflurane ; Metabolome ; Midazolam ; Oxygen ; Pulmonary Wedge Pressure ; Vecuronium Bromide

Phenobarbital is a long-acting barbiturate causing generalized depression of neuronal activity in the brain. Its effect is primarily achieved through enhanced GABA-mediated synaptic inhibition. Its use as an antiepileptic agent was first described in 1912. Before the introduction of phenytoin, phenobarbital is used as sedative-hypnotics. It is used for the treatment of epilepsy and status epilepticus. All barbiturates, including phenobarbital, have a high potential far abuse. They were frequently used for suicide attempts in the past, but they have in large part been replaced by benzodiazepines. the onset of symptoms depends on the drug and the route of administration. Mild to moderate barbiturate intoxication resembles ethanol inebriation with slurred speech, ataxia, and lethargy. Severe acute barbiturate intoxication is life threatening. Early deaths are generally cardiovascular-related. Hypotension, shock, pulmonary edema, and cardiac arrest that occurs with large doses are caused by depression of central sympathetic tone and as well as by direct depression of cardiac contractility. The potentially fatal oral dose of phenobarbital is 6-l0g. We describe an 23-year-old woman with pulmonary edema and cardiac arrest after ingestion of 18 grams of phenobarbital. She was completely recovered by successful cardiopulmonary resuscitation and hemoperfusion. We report a case with literature review.
Ataxia ; Barbiturates ; Benzodiazepines ; Brain ; Cardiopulmonary Resuscitation ; Depression ; Eating ; Epilepsy ; Ethanol ; Female ; Heart Arrest* ; Hemoperfusion ; Humans ; Hypotension ; Lethargy ; Neurons ; Phenobarbital* ; Phenytoin ; Pulmonary Edema* ; Shock ; Status Epilepticus ; Suicide ; Young Adult

Isoniazid(Isonicotinic acid hydrazide) is an antimicrobial drug used since 1952 as a fast line agent for the prophylaxis and treatment of tuberculosis. Isoniazid is well known for problems in population having a high prevalence of isoniazid use for prophylaxis or treatment of tuberculosis. But intentional or accidental isoniazid overdose is uncommon. The ingestion of toxic amounts of isoniazid causes recurrent seizures, profound metabolic acidosis, coma and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5g of isoniazid. Doses larder than 30mg per kg often produce seizures. When ingested in amounts of 80-150mg per kg or more, isoniazid can be rapid fatal. 40-year-old woman having previous pulmonary tuberculosis ingested 7 gram of isoniazid(140mg/kg) to attempt suicide approximately 30 minutes prior to visit to our emergency medical center. She had recurrent generalized tonicclonic seizures and metabolic acidosis. We report one patient treated with pyridoxine, which was equivalent to the amount of isoniazid ingested and administered as a intravenous dose and oral dose.
Acidosis ; Adult ; Coma ; Eating ; Emergencies ; Female ; Humans ; Isoniazid* ; Prevalence ; Pyridoxine ; Seizures* ; Suicide ; Tuberculosis ; Tuberculosis, Pulmonary

Serum myoglobin concentrations were studied in 46 patients during orthopedic and plastic operations that required the application of a pneumatic limb tourniquet. Serum myoglobin was measured at preoperation, during tourniquet and after touriquet release. In the general anesthesia patients, serum myoglobin was after tourniquet release(172.72+/-29.49 ng/ml) significantly increased(p<0.01) than at preoperation(103.06+/-24.03 ng/ml). In the regional block patients, serum myoglobin after tourniquet release(117.69+/-10.08ng/ml) also increased(p<0.05) than at preoperation(67.08+/-14.99ng/ml). In the male patients, serum myoglobin was significantly increased(p<0.05) during tourniquet and after tourniquet release(123.36+/-15.42ng/ml & 158.86+/-21.10ng/ml) than at preoperation (93.58+/-17.11ng/ml). In the female patients, there was no significant difference to regardless of tourniquet application. In the patients that tourniquet application time was within one hour, serum myoglohin was significantly increased(p<0.01) during tourniquet and after tourniquet release(125.66+/-18.86 & 126.20+/-14.99ng/ml) than at preoperation(86.12+/-15.29ng/ml). In the patients that tourniquet application time was over one hour, serum myoglobin was sig- nificantly increased(p<0.01) during tourniquet(l05.92+/-21.84ng/ml) than at preoperation(91.16+/-31.17ng/ml) and in the after tourniquet release(183.88+/-40.96ng/ml), serum myoglobin was more significantly(p<0.05) increased than during tourniquet.
Anesthesia, General ; Extremities ; Female ; Humans ; Male ; Myoglobin* ; Orthopedics ; Plastics ; Tourniquets*

BACKGROUND: Recent studies demonstrated that volatile anesthetics suppress the NO-cGMP system in the vascular system. It has been known that the hemodynamic changes produced by volatile anesthetics in septic patients are mediated by upregulation of iNOS leading to excessive release of NO. The mechanisms underlying suppression of the NO-cGMP system by anesthetics are still controversial. It has been elucidated that nitric oxide synthase (NOS) plays a major role in the regulatory function in the L-arginine-NO system. So we examined the effects of NOS inhibitor (L-NAME, aminoguanidine) and NO scavenger (hydroxocobalamin) on vascular smooth muscle contractile function in lipopolysaccharide (LPS)-treated rat aorta during halothane administration. METHODS: Aortic ring preparations were obtained from LPS-treated (1.5 mg/kg, ip, for 18 h) rats. We evaluated the effects of hydroxocobalamin, L-NAME and aminoguanidine on contractile responses to phenylephrine during halothane (1 & 2 MAC) administration respectively. Statistical significances (P<0.05) were analyzed according to data characterictics by repeated measures ANOVA test and student's t-test. RESULTS: The contractile responses to phenylephrine in LPS-treated rats aorta were significantly (P<0.05) increased in the presence of hydroxocobalamin and L-NAME. During the halothane (1 and 2 MAC) administration, the contractile responses to phenylephrine in LPS-treated rats aorta were increased significantly (P<0.05) in the presence of hydroxocobalamin and L-NAME. CONCLUSIONS: From these results, it is suggested that hydroxocobalamin and L-NAME may be useful in the therapy of septic shock.
Anesthetics ; Animals ; Aorta ; Halothane* ; Hemodynamics ; Humans ; Hydroxocobalamin* ; Muscle, Smooth, Vascular ; NG-Nitroarginine Methyl Ester* ; Nitric Oxide Synthase ; Phenylephrine ; Rats* ; Shock, Septic ; Up-Regulation

BACKGROUND: An endothelium derived vasoconstrictor peptide, endothelin, has been shown to be a potent coronary vascular constrictor. In the clinical settings of angina or myocardial ischemia, the endothelial injury of coronary artery can stimulate the endothelin production. In this study, the authors assessed the response to endothelin of the coronary artery in isolated rat heart and compared the relative effects of three vasodilators (nifedipine, adenosine, nitroprusside) on coronary vasospasm which was induced by endothelin. METHODS: The isolated rat heart preparations (Langendorff model) were obtained from fourty male Sprague-Dawley rats (350-400 gm). Preparations were perfusated with Krebs-Hanseleit solution of (mM): NaCl 115, NaHCO3 25, KCl 4.7, CaCl2 2H2O 2.5, MgCl2 6H2O 1.2, KH2PO4 1.2, glucose 10. The perfusate was maintained at 37oC and aerated with carbogen (oxygen 95% and carbon dioxide 5%). The coronary perfusion was maintained at 80 cmH20 pressure and Latex balloon was positioned in left ventricle. After the preparations were stabilized, endothelin (10(-9) M) was added to perfusate for 5 minutes and followed the perfusion without vasodilators (control, n = 10) or with vasodilators (nifedipine, adenosine and nitroprusside 10(-7) M to 10(-6) M, n = 10 each) for 45 minutes. The left ventricular developed pressure (LDP) and heart rate (HR) was recorded and the coronary effluent (VOL) was collected to measure the unit volume and the CPK isoenzyme (CK-MB). Effects of the interventions were assessed using analysis of variance. All values are presented as means +/- SE. RESULTS: VOL, HR and VDP were significantly reduced after infusion of 10(-9) M endothelin in 3 and 5 minutes. VOL was recovered efficiently after infusion of three vasodilators. Adenosine and nitroprusside groups showed superior recovery in the changes of rate pressure product (RPP) than in nifedipine group, which was significant reduced in VDP. CONCLUSIONS: These results suggest that in the situation of endothelin induced severe coronary vasospasm, adenosine and nitroprusside effectively reversed the coronary vasospasm without severe myocardial depression.
Adenosine ; Animals ; Carbon Dioxide ; Coronary Vasospasm* ; Coronary Vessels ; Depression ; Endothelins* ; Endothelium ; Glucose ; Heart Rate ; Heart Ventricles ; Heart* ; Humans ; Latex ; Magnesium Chloride ; Male ; Myocardial Ischemia ; Nifedipine ; Nitroprusside ; Perfusion ; Rats* ; Rats, Sprague-Dawley ; Vasodilator Agents*