BACKGROUND: This study aimed to investigate bradycardia as an adverse effect after administration of dexmedetomidine during 33degrees C target temperature management. METHODS: A retrospective study was conducted on patients who underwent 33degrees C target temperature management in the emergency department during a 49-month study period. We collected data including age, sex, weight, diagnosis, bradycardia occurrence, target temperature management duration, sedative drug, and several clinical and laboratory results. We conducted logistic regression for an analysis of factors associated with bradycardia. RESULTS: A total of 68 patients were selected. Among them, 39 (57.4%) showed bradycardia, and 56 (82.4%) were treated with dexmedetomidine. The odds ratio for bradycardia in the carbon monoxide poisoning group compared to the cardiac arrest group and in patients with higher body weight were 7.448 (95% confidence interval [CI] 1.834-30.244, p = 0.005) and 1.058 (95% CI 1.002-1.123, p = 0.044), respectively. In the bradycardia with dexmedetomidine group, the infusion rate of dexmedetomidine was 0.41 +/- 0.15 microg/kg/h. Decisions of charged doctor's were 1) slowing infusion rate and 2) stopping infusion or administering atropine for bradycardia. No cases required cardiac pacing or worsened to asystole. CONCLUSIONS: Despite the frequent occurrence of bradycardia after administration of dexmedetomidine during 33degrees C target temperature management, bradycardia was completely recovered after reducing infusion rate or stopping infusion. However, reducing the infusion rate of dexmedetomidine lower than the standard maintenance dose could be necessary to prevent bradycardia from developing in patients with higher body weight or carbon monoxide poisoning during 33degrees C targeted temperature management.
Atropine ; Body Weight ; Bradycardia* ; Carbon Monoxide Poisoning ; Dexmedetomidine* ; Diagnosis ; Emergency Service, Hospital ; Heart Arrest ; Humans ; Hypothermia, Induced ; Logistic Models ; Odds Ratio ; Retrospective Studies

Following results were obtained from the light microscopic and stereomicroscopic observations of the breasts of rats treated with 9, 10-Dimethyl-1,2-Benzanthracene(DMBA). 1) Adenocarcinomas developed in 17 rats (24%) among 70 DMBA-treated rats. 2) Terminal and buds (TEB) were observed longer in DMBA-treated rats than in control group, but they finally disppeared 4 monthes after treatment. 3) Many hyperplastic alveolar nodules (HAN) developed in DMBA-treated rats. 4) There were no transitional lesions between TEB and adenocarcinoma or HAN and adenocarcinoma. 5) The number of lobules was decreased in DMBA-treated rats. On the other hand, terminal ducts were increased in number. These findings suggest that DMBA stimulate the regression of lobules and induce to form terminal ducts from which adenocarcinomas and HAN develop independently.
Rats ; Animals ; Adenocarcinoma ; Breast Neoplasms

In contrast to the nodular renal blastema which is defined by nests of primitive metanephric cells after 36 weeks of gestation, the nephroblastomatosis is characterized by neoplastic proliferation of the primitive cells. This lesion is presumed to be closely related to the development of Wilms' tumor. We report a case of bilateral nephroblastomatosis associated with Wilms' tumor in a child. This 4 1/2 year-old girl was admitted because of a 10 cm-sized round mass in the right kidney, and smaller nodules in the left kidney and the lung. After three cycles of chemotherapy and subsequent disappearance of the nodules in the left kidney and lung, she underwent a right nephrectomy and a wedge resection of the left kidney. A round Wilms' tumor mass was seen in the lower pole of the right kidney. Remaining right renal cortex showed multiple, slightly depressed gray-white nodules associated with multiple samll cysts. They were comprised of multifocal subcapsular nests of primitive nephrogenic cells with focal tubular or glomerular differentiation. They resembled fetal renal tissue. In the left kidney, similar nests of primitive cells were also noted. These lesions were interpreted as multifocal perilobar type of nephroblastomatosis.
Child ; Male ; Female ; Humans

INTRODUTION: The gamma-aminobutyric acid type A (GABAA) receptor is an important pharmacological target of alcohol. The phamacological characteristics of the receptor are largely determined by its subunit composition. Compared with all other alpha subtypes, the alpha6- containing receptors are more sensitive to GABA and less sensitive to benzodiazepines. The purpose of this study was to address a role for GABAAalpha6 receptor subunit gene in the development of alcohol dependence. The differential manifestation of alcohol withdrawal symptoms related to GABAAalpha6 polymorphism in patients treating with benzodiazepines was also examined. METHODS: Eighty-seven inpatients with alcohol dependence, and sixty healthy controls were evaluated using CIWA-Ar scale. Each patient was genotyped for GABAAalpha6 subunit. Association between GABAAalpha6 polymorphism and severity of withdrawal symptom were determined. RESULTS: No significant difference was found in GABAAalpha6 receptor genetic type and allelic distribution between the alcohol dependent and control subject. Tremor was more severe in CC than TT type. TT type had higher degree of anxiety, agitation and headache than CC type. The GABAAalpha6 C allele increased the average score of tremor significantly, and T allele increased that of agitation. CONCLUSION: The results suggested that GABAAalpha6 genetic polymorphism was not associated with alcohol dependence and with severity of alcohol withdrawal symptoms. But in benzodiazepine treated patients, GABAAalpha6 polymorphism and allelic type show the difference in severity of each withdrawal symptom. These differences of severity are partly responsible for the unique pharmacological properties associated with the GABAAalpha6 subunit.
Alcoholism ; Alleles ; Anxiety ; Benzodiazepines ; Dihydroergotamine ; gamma-Aminobutyric Acid ; Headache ; Humans ; Inpatients ; Polymorphism, Genetic ; Receptors, GABA ; Substance Withdrawal Syndrome* ; Tremor

A 63-year-old man complained of intermittent motor weakness of his arm. The magnetic resonance image (MRI) of his brain displayed a high signal lesion in right cingulate gyrus on T2 weighted image. One year later, he showed a stuporous mental status with repeated seizures, and the follow-up brain MRI showed heterogeneously enhanced mass associated with bleeding. He was treated with surgery and radiotherapy for secondary glioblastomas in right cingulate gyrus. One year more later, a mass recurred on the left frontal base, and gliosarcoma was diagnosed. After tumor resection, ventriculoperitoneal shunt, chemotherapy, and re-radiation therapy, all brain lesions were stable. Fourteen months after the diagnosis of gliosarcoma, he complained of dyspnea and back pain. Torso positron emission tomography/computed tomography revealed multiple metastatic lesions in both lungs, pericardium, pleura, liver, lymph nodes, and bones, and metastatic gliosarcoma was diagnosed. One month later, the patient died because of the systemic metastases. We present an unusual case of secondary gliosarcoma with stable brain lesions and extensive systemic metastases.
Arm ; Back Pain ; Brain ; Brain Neoplasms ; Diagnosis ; Drug Therapy ; Dyspnea ; Electrons ; Follow-Up Studies ; Glioblastoma ; Gliosarcoma* ; Gyrus Cinguli ; Hemorrhage ; Humans ; Liver ; Lung ; Lymph Nodes ; Magnetic Resonance Imaging ; Middle Aged ; Neoplasm Metastasis* ; Pericardium ; Pleura ; Radiotherapy ; Seizures ; Stupor ; Torso ; Ventriculoperitoneal Shunt

PURPOSE: Febrile convulsions (FC) were considered to be a benign seizure syndrome that is distinct from epilepsy. But it is thought that children with complex features i.e., partial or prolonged seizures or multiple episodes of FC would bear a higher risk of developing unprovoked seizures. The aim of this study is to look into the relative significance of each criteria that define complex febrile convulsions (CFC) as a predictor of subsequent epilepsy. METHODS: All children were retrospectively identified for a febrile seizure through pediatric departments of the Konyang University Hospital. Information was collected from medical records and interviews with parents. Patients with abnormal neurological examinations at presentation were excluded. RESULTS: This study was performed from March 2000 to December 2003. Sixty-three out of 314 children (20.0%) with febrile convulsion fulfilled the criteria for CFC and forty-four children of them have been followed for 12 months or more. Ten of these (23.2%) had unprovoked seizures for 14-62 months (median 34.2+/-11.6 months). The patients with partial FC showed a trend toward a higher risk (57.1%) of developing epilepsy than the patients with multiple or prolonged febrile convulsions (26.7%, 24.1% respectively). CONCLUSION: We found that the partial feature of febrile convulsion is associated with subsequent epilepsy.
Child* ; Epilepsy ; Humans ; Medical Records ; Neurologic Examination ; Parents ; Retrospective Studies ; Seizures* ; Seizures, Febrile*

The MHC class II transactivator (CIITA) is the master transcriptional regulator of genes involved in MHC class II restricted antigen presentation. Previously we suggested another role of CIITA in Th1/Th2 balance by demonstrating that forced expression of CIITA in murine T cells repressed Th1 immunity both in vitro and in vivo. However, the results were contradictory to the report that CIITA functioned to suppress the production of Th2 cytokine by CD4+T cells in CIITA deficient mice. In this study, we investigated the influence of constitutive expression of CIITA in T cells on Th2 immune response in vivo using murine experimental colitis model. In the dextran sodium sulfate-induced acute colitis, a disease involving innate immunity, CIITA transgenic mice and wild type control mice showed similar progression of the disease. However, the development of oxazolone-induced colitis, a colitis mediated by predominantly Th2 immune response, was aggravated in CIITA-transgenic mice. And, CD4+T cells from the mesenteric lymph node of CIITA-transgenic mice treated with oxazolone exhibited a high level of IL-4 secretion. Together, these data demonstrate that constitutive expression of CIITA in T cells skews immune response to Th2, resulting in aggravation of Th2-mediated colitis in vivo.
Trans-Activators/*physiology ; Th2 Cells/*immunology ; T-Lymphocytes/*metabolism ; Oxazolone/pharmacology ; Nuclear Proteins/*physiology ; Mice, Transgenic ; Mice, Inbred C57BL ; Mice ; Interleukin-4/biosynthesis ; Colitis/*etiology ; Animals

Paralytic shellfish poisoning results from consumption of mollusks that have fed on dinoflagellates capable of producing neurotoxins such as saxitoxin. The saxitoxin is concentrated in the shellfish and acts by decreasing sodium-channel permeability, thereby blocking neuronal transmission in skeletal muscles. Symptoms including paresthesia, perioral numbness, perioral tingling, nausea, vomiting, extremity numbness, extremity tingling, dizziness, ataxia, dysphagia, and weakness have been reported. In serious cases, respiratory hold may occur up to 6~24 hours after ingestion. Generally, the treatment for paralytic shellfish poisoning is supportive care, but mechanical ventilation is needed in serious cases acompanied by respiratory hold. We experienced two cases of paralytic shellfish poisoning. Respiratory hold was presented in one case and only mild paresthesia in the other case. After supportive management, including mechanical ventilation in former case, both patients were discharged without sequalae.
Ataxia ; Deglutition Disorders ; Dinoflagellida ; Dizziness ; Eating ; Extremities ; Humans ; Hypesthesia ; Mollusca ; Muscle, Skeletal ; Nausea ; Neurons ; Neurotoxins ; Paresthesia ; Permeability ; Respiration, Artificial ; Saxitoxin* ; Shellfish ; Shellfish Poisoning* ; Vomiting

After endoscopic treatment of common bile duct (CBD) stones, recurrence of choledocholithiasis due to small stone fragments and post-endoscopic retrograde cholangiopancreatography (post-ERCP) cholangitis can occur. We determined the effect of biliary stenting after removal of CBD stones on the recurrence of CBD stones and the incidence of post-ERCP cholangitis. Methods: We performed a retrospective single-center study involving 483 patients who underwent ERCP for the removal of CBD stones. The patients were classified into two groups according to their biliary stenting status. The primary outcome was the rate of CBD stone recurrence and the secondary outcome was the incidence of post-ERCP cholangitis. Results: Among the 483 patients, 219 and 264 did and did not receive a biliary stent after CBD stone removal, respectively. The incidence of stone recurrence was 15.5% and 7.6% in the non-stenting and stenting groups (p = 0.006), respectively, while the incidence of post-ERCP cholangitis was 4.6% and 2.7% (p = 0.256). In a multivariate analysis, biliary stenting significantly reduced the stone recurrence rate (odds ratio, 0.30; p = 0.004). Conclusions: Biliary stenting after the removal of CBD stones reduces the stone recurrence rate and assisted recovery. For patients with large and multiple stones who undergo lithotripsy, preventive biliary stent insertion can reduce the rate of stone recurrence.

Although various functions of CD99 have been reported, such as apoptosis and homotypic aggregation of thymocyte and transendothelial migration of immune cells, biochemical/molecular natures of CD99 are still elusive. Using mouse CD99 gene, we show that CD99 forms homodimer through its extracellular domain. Expression of mouse CD99 is up-regulated on T cells after CD3-mediated activation, like the case for human CD99. The potential of CD99 to form homodimer was tested with a recently developed bimoleular fluorescence complementation analysis (BiFC). In BiFC analysis, the dimerization-induced fluorescence was strong near the perinuclear region and was faded at the cell membrane. However, surface expression of CD99 was still detected by flow cytometry, suggesting that CD99 either in monomer form or in association with other molecules exists on the cell surface. In BiFC analysis using CD99 mutants with its extracellular, transmembrane, or cytosolic domains changed to corresponding human CD4 domains, the mutant replaced with human CD4-extracellular domain did not produce fluorescence. Purified soluble CD99-Fc fusion proteins bound to CD99-Fc immobilized onto the gold sensor chip in surface plasmon resonance analysis, confirming that the extracellular domain was responsible for dimer formation. Intracytoplasmic staining for CD99 expression in the thymocytes and mature T cells showed that most of the cells, even the cells with low surface level of CD99, contained the molecule inside the cell. Our results suggest that majority of CD99 homodimers may exit in the cell and be exported to the cell surface, dissociating from each other, after a certain regulatory signal is delivered.
Animals ; Antigens, CD/chemistry/*isolation & purification ; Cell Adhesion Molecules/chemistry/*isolation & purification ; Flow Cytometry ; *Fluorescence ; Luminescent Measurements/*methods ; Mice ; Molecular Biology/*methods ; T-Lymphocytes/immunology