Diagnostic Analysis of Patients with Essential Hypertension Using Association Rule Mining / 대한의료정보학회지

OBJECTIVES: The purpose of this study was to analyze the records of patients diagnosed with essential hypertension using association rule mining (ARM). METHODS: Patients with essential hypertension (ICD code, I10) were extracted from a hospital's data warehouse and a data mart constructed for analysis. Apriori modeling of the ARM method and web node in the Clementine 12.0 program were used to analyze patient data. RESULTS: Patients diagnosed with essential hypertension totaled 5,022 and the diagnostic data extracted from those patients numbered 53,994. As a result of the web node, essential hypertension, non-insulin dependent diabetes mellitus (NIDDM), and cerebral infarction were shown to be associated. Based on the results of ARM, NIDDM (support, 35.15%; confidence, 100%) and cerebral infarction (support, 21.21%; confidence, 100%) were determined to be important diseases associated with essential hypertension. CONCLUSIONS: Essential hypertension was strongly associated with NIDDM and cerebral infarction. This study demonstrated the practicality of ARM in co-morbidity studies using a large clinic database.

Effect of the K+ Channel Modulations on Glutamate and K+ Concentrations in Rabbit Hippocampus during Transient Global Ischemia / 대한마취과학회지

BACKGROUND: Cerebral ischemia causes an increase in extracellular potassium ([K+]e) through activation of the KATP channel. This increase in [K+]e could result in neuronal depolarization and a reversal of the glutamate uptake system in glia. This may further contribute to the excessive concentrations of glutamate and asparate in the extracellular space during ischemia. If the early rise in [K+]e during ischemia could be attenuated, less excitotoxic neuronal damage may be the result. However, activation of KATP channels has been shown to attenuate the anoxia induced depolarization in the hippocampus and may reduce the release of excitatory neurotransmitters during cerebral ischemia. In this study, we address the question of whether KATP channel modulation affects [K+]e and whether it is related with extracellular glutamate concentrations. METHODS: After approval by the Animal Care and Use Committee, 18 New Zealand white rabbits were anesthetized with halothane and mechanically ventilated to maintain normocarbia. Microdialysis catheters were inserted into the left dorsal hippocampus and perfused with artificial cerebrospinal fluid at 2 ml/min. K+ sensitive microelectrodes were inserted into the contralateral hippocampus. A pneumatic tourniquet was placed loosely around the neck. Animals were randomized to receive glibenclamide (n=5, KATP blocker, 3.7 mg/kg) or cromakalim (n=5, KATP opener, 0.5 mg/kg). The control group (n=6) had neither drug. Ten-minute period of global cerebral ischemia was produced by inflation of the tourniquet combined with induced hypotension. Hippocampal [K+]e was measured throughout the periischemic period and glutamate concentrations in dialysate were determined by high-performance liquid chromatography. Peak levels were compared by ANOVA. RESULTS: Glutamate concentration significantly increased during ischemia period for all groups (p<0.05). In glibenclamide treated animals, brain glutamate concentration increased markedly during early reperfusion (t=I+15) compared to other groups (p<0.05). There were no statistical differences on ischemia-induced increases in [K+]e among the three groups. CONCLUSIONS: Although it was not possible to demonstrate an effect of modulators of the ATP sensitive K+ channel on [K+]e, glibenclamide increased glutamate during reperfusion. This paradoxical increase in glutamate after administration of a K+ channel blocker suggests that the mechanism of glutamate release is not related to [K+]e change.