In patients with epilepsy, depression is a common comorbidity but difficult to be treated because many antidepressants cause pro-convulsive effects. Thus, it is important to identify the risk of seizures associated with antidepressants. To determine whether paroxetine, a very potent selective serotonin reuptake inhibitor (SSRI), interacts with ion channels that modulate neuronal excitability, we examined the effects of paroxetine on Kv3.1 potassium channels, which contribute to highfrequency firing of interneurons, using the whole-cell patch-clamp technique. Kv3.1 channels were cloned from rat neurons and expressed in Chinese hamster ovary cells. Paroxetine reversibly reduced the amplitude of Kv3.1 current, with an IC₅₀ value of 9.43 µM and a Hill coefficient of 1.43, and also accelerated the decay of Kv3.1 current. The paroxetine-induced inhibition of Kv3.1 channels was voltage-dependent even when the channels were fully open. The binding (k₊₁) and unbinding (k₋₁) rate constants for the paroxetine effect were 4.5 µM⁻¹s⁻¹ and 35.8 s⁻¹, respectively, yielding a calculated K(D) value of 7.9 µM. The analyses of Kv3.1 tail current indicated that paroxetine did not affect ion selectivity and slowed its deactivation time course, resulting in a tail crossover phenomenon. Paroxetine inhibited Kv3.1 channels in a usedependent manner. Taken together, these results suggest that paroxetine blocks the open state of Kv3.1 channels. Given the role of Kv3.1 in fast spiking of interneurons, our data imply that the blockade of Kv3.1 by paroxetine might elevate epileptic activity of neural networks by interfering with repetitive firing of inhibitory neurons.
Animals ; Antidepressive Agents ; Clone Cells ; Comorbidity ; Cricetinae ; Cricetulus ; Depression ; Epilepsy ; Female ; Fires ; Humans ; Interneurons ; Ion Channels ; Neurons ; Ovary ; Paroxetine* ; Patch-Clamp Techniques ; Rats ; Seizures ; Serotonin ; Shaw Potassium Channels* ; Tail

Bacillus (B.) anthracis is the pathogen that causes fatal anthrax. Strain-specific detection of this bacterium using molecular approaches has enhanced our knowledge of microbial population genetics. In the present study, we employed molecular approaches including multiple-locus variable-number tandem repeat analysis (MLVA) and canonical single-nucleotide polymorphism (canSNP) analysis to perform molecular typing of B. anthracis strains isolated in Korea. According to the MLVA, 17 B. anthracis isolates were classified into A3a, A3b, and B1 clusters. The canSNP analyses subdivided the B. anthracis isolates into two of the three previously recognized major lineages (A and B). B. anthracis isolates from Korea were found to belong to four canSNP sub-groups (B.Br.001/2, A.Br.005/006, A.Br.001/002, and A.Br.Ames). The A.Br.001/002 and A.Br.Ames sub-lineages are closely related genotypes frequently found in central Asia and most isolates were. On the other hand, B. anthracis CH isolates were analyzed that belonged to the B.Br.001/002 sub-group which found in southern Africa, Europe and California (USA). B.Br.001/002 genotype is new lineage of B. anthracis in Korea that was not found before. This discovery will be helpful for the creation of marker systems and might be the result of human activity through the development of agriculture and increased international trade in Korea.
Africa, Southern ; Agriculture ; Anthrax ; Asia ; Bacillus ; Bacillus anthracis ; California ; Europe ; Genetics, Population ; Genotype ; Hand ; Human Activities ; Molecular Typing ; Tandem Repeat Sequences

A 50-year-old man presented with acute pancreatitis. Abdominal CT showed cystic dilatation of common bile duct and diffuse dilatation of pancreatic duct. ERCP showed pancreas divisum, choledochal cyst and pancreatic duct stones. Minor papilla sphincterotomy and insertion of nasopancreatic tube were performed for drainage of dorsal pancreatic duct. And then, he underwent Whipples operation for excision of choledochal cyst and decompresion of dorsal pancreatic duct.
Cholangiopancreatography, Endoscopic Retrograde ; Choledochal Cyst* ; Common Bile Duct ; Dilatation ; Drainage ; Humans ; Middle Aged* ; Pancreas* ; Pancreatic Ducts ; Pancreatitis ; Tomography, X-Ray Computed

BACKGROUND/AIMS: Genetic variations of ethanol-metabolizing enzymes can affect alcohol drinking behavior. The aims of this study were to investigate and compare the distributions of these genetic polymorphisms between a healthy control group and a heavy drinker group which included an alcoholic liver cirrhosis group. METHODS: Genotypes of ADH2, ALDH2, CYP2E1, and catalase were identified by polymerase chain reaction and restriction fragment length polymorphism. Genomic DNA was extracted from peripheral leukocytes in 42 healthy controls, 12 heavy drinkers, and 30 alcoholic liver cirrhosis patients. RESULTS: 1) The genotype frequencies of ALDH2 (1*1), ADH2 (1*1), CYP2E1 (c1c1), and catalase1 (TT) were 69%, 55%, 38%, and 12%, respectively in healthy Korean males. 2) There was a significant difference in the distribution of the genetic polymorphism of ALDH2 between the control group and heavy drinker group (12 heavy drinkers and 30 alcoholic liver cirrhosis patients). The genotype frequency of ALDH2 mutant, ALDH2 (1*2) and ALDH2 (2*2) in the heavy drinker group (12%) was significantly lower than that in the control group (30%). 3) We didn't find anyone with ALDH2 homozygote mutant (DD) in the heavy drinker group. 4) There was no significant difference in the distribution of genetic polymorphisms in ADH2, CYP2E1 and catalase1 between the two groups. CONCLUSIONS: These results suggest that the absence of ALDH2 mutant genotype is strongly related to heavy drinking behavior. We can not prove, however, any evidence that the polymorphisms of other ethanol-metabolizing enzymes are associated with the determination of alcohol-drinking behavior.
Adult ; Alcohol Dehydrogenase/*genetics ; Alcohol Drinking ; Alcoholism/enzymology/*genetics ; Aldehyde Dehydrogenase/*genetics ; Cytochrome P-450 CYP2E1/*genetics ; Ethanol/metabolism ; Humans ; Liver Cirrhosis, Alcoholic/enzymology/*genetics ; Male ; Middle Aged ; *Polymorphism, Genetic

Eosinophilic gastroenteritis is a rare disorder of unknown origin that is pathologically characterized by marked infiltration of eosinophils in the wall of the gastrointestinal tracts. Eosinophilic gastroenteritis is often classified according to the layer of the bowel wall involved. We experienced two cases of eosinophilic gastroenteritis. One case having whole small bowel wall involvement resulting in small bowel obstruction and eosinophilic ascites underwent bowel resection followed by oral steroid treatment. The other case having mucosal layer involvement with chronic diarrhea and hypoalbuminemia was treated with oral corticosteroid and responded dramatically. In addition, we report one case of hypereosinophilic syndrome involving the gastrointestinal tracts. The patient presented with abdominal pain, ascites, and urticaria. and also showed good response to oral steroid.
Abdominal Pain ; Ascites ; Diarrhea ; Eosinophils* ; Gastroenteritis* ; Gastrointestinal Tract ; Humans ; Hypereosinophilic Syndrome* ; Hypoalbuminemia ; Urticaria

Jejunal infarction as a complication of acute pancreatitis is not common and can not be well recognized. This jejunal infarction usually arises from the venous thrombosis rather than arterial thrombosis. Jejunal infarction results in bowel perforation or stenosis according to its extension of injury and progression rate. Pathologic findings of the involved jejunum show a segmental transmural infarction and mesenteric venous thrombotic occlusions. Early diagnosis should be made for better prognosis. We report a patient with jejunal infarction resulting perforation due to acute pancreatitis, in which the initial presenting symptoms were hematemesis and abdominal distention.
Acute Disease ; Adult ; English Abstract ; Humans ; Infarction/diagnosis/*etiology ; Intestinal Perforation/diagnosis/*etiology ; Jejunal Diseases/diagnosis/*etiology ; Jejunum/*blood supply ; Male ; Pancreatitis/*complications ; Rupture, Spontaneous

OBJECTIVES: Calcium salts are usually present in the center of all types of gallstones, including pure cholesterol stones. It has been postulated that precipitation of calcium salts might act as a nidus for gallstone formation. Our goal was to determine whether a calcium-binding protein was present in bile and whether this protein has any calcium-binding properties. METHODS: Calcium-binding moiety was obtained by addition of CaC12 into the gallbladder bile. Calcium-binding protein was identified by SDS-PAGE (sodium dodecyl sulfate-polyacrylamide gel electrophoresis). The capacity to bind calcium was confirmed by autoradiography with 45Ca++. RESULTS: We identified a protein(M.W. Autoradiography ; Bile* ; Calcium ; Cholesterol ; Electrophoresis, Polyacrylamide Gel ; Gallbladder* ; Gallstones ; Humans ; Salts

BACKGROUND AND PURPOSE: Decreasing the time delay for thrombolysis, including intravenous thrombolysis (IVT) with tissue plasminogen activator and intra-arterial thrombectomy (IAT), is critical for decreasing the morbidity and mortality of patients experiencing acute stroke. We aimed to decrease the in-hospital delay for both IVT and IAT through a multidisciplinary approach that is feasible 24 h/day. METHODS: We implemented the Stroke Alert Team (SAT) on May 2, 2016, which introduced hospital-initiated ambulance prenotification and reorganized in-hospital processes. We compared the patient characteristics, time for each step of the evaluation and thrombolysis, thrombolysis rate, and post-thrombolysis intracranial hemorrhage from January 2014 to August 2016. RESULTS: A total of 245 patients received thrombolysis (198 before SAT; 47 after SAT). The median door-to-CT, door-to-MRI, and door-to-laboratory times decreased to 13 min, 37.5 min, and 8 min, respectively, after SAT implementation (P<0.001). The median door-to-IVT time decreased from 46 min (interquartile range [IQR] 36–57 min) to 20.5 min (IQR 15.8–32.5 min; P<0.001). The median door-to-IAT time decreased from 156 min (IQR 124.5–212.5 min) to 86.5 min (IQR 67.5–102.3 min; P<0.001). The thrombolysis rate increased from 9.8% (198/2,012) to 15.8% (47/297; P=0.002), and the post-thrombolysis radiological intracranial hemorrhage rate decreased from 12.6% (25/198) to 2.1% (1/47; P=0.035). CONCLUSIONS: SAT significantly decreased the in-hospital delay for thrombolysis, increased thrombolysis rate, and decreased post-thrombolysis intracranial hemorrhage. Time benefits of SAT were observed for both IVT and IAT and during office hours and after-hours.
Ambulances ; Cerebral Infarction ; Humans ; Intracranial Hemorrhages ; Mortality ; Stroke* ; Thrombectomy ; Thrombolytic Therapy ; Tissue Plasminogen Activator