Objective: Mild cognitive impairment (MCI) is considered a pre-stage of dementia. This study aims to develop a cognitive intervention treatment program (CITP) as a non-pharmacological therapy, apply this program into MCI patients, and examine patients’ changes in cognitive function. Methods: Among 16 patients with MCI, 10 patients were randomly assigned to the experimental group and 6 patients were assigned into the control group. The patients assigned to the experimental group participated in the CITP once a week for a period of 15 weeks.The control group were suggested to live a normal daily life without CITP given. After 15 weeks (3 months), pre- and post-investigations, such as cognitive function test, emotional test, brain oxygen saturation test, were conducted and compared for each group. Results: The cognitive function scores and the brain oxygen saturation levels taken during the Verbal Fluency Test showed a sta-tistically significant difference between those of experimental and the control groups. To be specific, while the cognitive function score improved in the experimental group, there was a decline in the control group. There was no statistically significant difference in emo-tional changes between two groups. Looking at the changes within each group, the overall cognitive function score of the experimen-tal group was significantly increased, but no pre- and post-significantly changes were observed in brain oxygen saturation activation. On the other hand, the control group showed a statistically significant decline in the attention criteria of the cognitive functional ar-eas, and no statistically significant changed in brain activation. Conclusion The result from this study has given some promising views on maintaining and improving the deteriorating cognitive function in patients with MCI. Conducting CITP on patients is expected to strengthen the neural network. Eventually, there would be a less deterioration of cognitive function and less progression of MCI into dementia.

Background and Objectives: Nonalcoholic fatty liver disease (NAFLD) is an excessiveaccumulation of fat into the liver as a result of increased inflammation and insulin resistance.Although there can be common pathogenic mechanisms for NAFLD and hypertensionassociated with the development of cardiovascular diseases, little data are showing theassociation between NAFLD and hypertension in a large-scale cohort study. Thus, weevaluated the ability of the fatty liver index (FLI), a surrogate marker of NAFLD, to predict thedevelopment of hypertension in healthy individuals. Methods: We included 334,280 healthy individuals without known comorbidities whounderwent the National Health check-ups in South Korea from 2009 to 2014. Theassociation between the FLI and hypertension was analyzed using multivariate Coxproportional-hazards models. Results: During a median of 5.2 years' follow-up, 24,678 subjects (7.4%) had new-onsethypertension. We categorized total subjects into quartile groups according to FLI (range: Q1,0–4.9; Q2, 5.0–12.5; Q3, 12.6–31.0; and Q4, >31.0). The incidence of hypertension was higherin subjects with the highest FLI than in those with the lowest FLI (Q4, 9,968 [11.9%] vs. Q1,2,277 [2.7%]; p<0.001). There was a significant correlation between the highest FLI and anincreased risk of new-onset hypertension (adjusted hazard ratio between Q4 and Q1, 2.330;95% confidence interval, 2.218–2.448; p<0.001). FLI was significantly associated with anincreased risk of new-onset hypertension regardless of baseline characteristics. Conclusions Higher FLI was independently associated with increased risk of hypertension ina healthy Korean population.

There are limited data on the impact of diabetes control on the risk of subclinical coronary atherosclerosis.

BACKGROUND AND OBJECTIVES: We sought to evaluate nationwide trends, characteristics, and clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) in Korea. METHODS: From National Health Insurance claims data in Korea, 81,115 patients, who underwent PCI for the first episode of coronary artery disease between 2011 and 2015, were enrolled. Patients were categorized into angina (n=49,288) or acute myocardial infarction (AMI, n=31,887) groups and analyzed. RESULTS: The mean age of patients was 64.4±12.2 years and 56,576 (69.7%) were men. Diabetes, hyperlipidemia, and hypertension were observed in 27,086 (33.4%), 30,675 (37.8%), and 45,389 (56.0%) patients, respectively. There was a 10% increase in the number of patients undergoing PCI for angina between 2011–2012 and 2014–2015 (11,105 vs. 13,261; p=0.021). However, the number of patients undergoing PCI for AMI marginally decreased between 2011–2012 and 2014–2015 (8,068 vs. 7,823; p=0.052). In procedures, drug-eluting stent was the most frequently used device (93.2%), followed by balloon angioplasty (5.5%) and bare metal stents (1.3%). The mean number of stents per patient was 1.39±0.64. At discharge, dual-anti platelet therapy, statin, beta-blockers, and angiotensin converting enzyme inhibitor or angiotensin receptor blocker were provided to 76,292 (94.1%), 71,411 (88.0%), 57,429 (70.8%), and 54,418 (67.1%) patients, respectively. The mean in-hospital and 1-year total medical costs were 8,628,768±4,832,075 and 13,128,158±9,758,753 Korean Won, respectively. In-hospital mortality occurred in 2,094 patients (2.6%). CONCLUSIONS: Appropriate healthcare strategies reflecting trends, characteristics, and clinical outcomes of PCI are needed in Korea.
Angina Pectoris ; Angioplasty, Balloon ; Angiotensins ; Blood Platelets ; Coronary Artery Disease ; Delivery of Health Care ; Drug-Eluting Stents ; Hospital Mortality ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hyperlipidemias ; Hypertension ; Korea ; Male ; Myocardial Infarction ; National Health Programs ; Peptidyl-Dipeptidase A ; Percutaneous Coronary Intervention ; Stents

BACKGROUND AND OBJECTIVES: We sought to evaluate nationwide trends, characteristics, and clinical outcomes in patients undergoing percutaneous coronary intervention (PCI) in Korea. METHODS: From National Health Insurance claims data in Korea, 81,115 patients, who underwent PCI for the first episode of coronary artery disease between 2011 and 2015, were enrolled. Patients were categorized into angina (n=49,288) or acute myocardial infarction (AMI, n=31,887) groups and analyzed. RESULTS: The mean age of patients was 64.4±12.2 years and 56,576 (69.7%) were men. Diabetes, hyperlipidemia, and hypertension were observed in 27,086 (33.4%), 30,675 (37.8%), and 45,389 (56.0%) patients, respectively. There was a 10% increase in the number of patients undergoing PCI for angina between 2011–2012 and 2014–2015 (11,105 vs. 13,261; p=0.021). However, the number of patients undergoing PCI for AMI marginally decreased between 2011–2012 and 2014–2015 (8,068 vs. 7,823; p=0.052). In procedures, drug-eluting stent was the most frequently used device (93.2%), followed by balloon angioplasty (5.5%) and bare metal stents (1.3%). The mean number of stents per patient was 1.39±0.64. At discharge, dual-anti platelet therapy, statin, beta-blockers, and angiotensin converting enzyme inhibitor or angiotensin receptor blocker were provided to 76,292 (94.1%), 71,411 (88.0%), 57,429 (70.8%), and 54,418 (67.1%) patients, respectively. The mean in-hospital and 1-year total medical costs were 8,628,768±4,832,075 and 13,128,158±9,758,753 Korean Won, respectively. In-hospital mortality occurred in 2,094 patients (2.6%). CONCLUSIONS Appropriate healthcare strategies reflecting trends, characteristics, and clinical outcomes of PCI are needed in Korea.

This study attempted to calculate and investigate the incidence of hospitalized acute myocardial infarction (AMI) and stroke in Korea. Using the National Health Insurance claim data, we investigated patients whose main diagnostic codes included AMI or stroke during 2006 to 2010. As a result, we found out that the number of AMI hospitalized patients had decreased since 2006 and amounted to 15,893 in 2010; and that the number of those with stroke had decreased since 2006 and amounted to 73,501 in 2010. The age-standardized incidence rate of hospitalized AMI, after adjustment for readmission, was 41.6 cases per 100,000-population in 2006, and had decreased to 29.4 cases in 2010 (for trend P < 0.001). In the case of stroke was estimated at 172.8 cases per 100,000-population in 2006, and had decreased to 135.1 cases in 2010 (for trend P < 0.001). In conclusion, the age-standardized incidence rates of both hospitalized AMI and stroke in Korea had decreased continuously during 2006 to 2010. We consider this decreasing trend due to the active use of pharmaceuticals, early vascular intervention, and the national cardio-cerebrovascular disease care project as the primary and secondary prevention efforts.
Acute Disease ; Adolescent ; Adult ; Age Factors ; Aged ; Aged, 80 and over ; Child ; Child, Preschool ; Female ; Hospitalization/*trends ; Humans ; Incidence ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Myocardial Infarction/*epidemiology ; Patient Readmission ; Republic of Korea/epidemiology ; Sex Factors ; Stroke/*epidemiology ; Young Adult

BACKGROUND: Small vessel dementia (SVD) is the most frequent cause of vascular dementia and is regarded a distinct clinical entity. However, the data on the natural course of SVD and drug trials specifically aiming SVD have been sparse. The aim of this study was to answer the following three questions: 1) How does SVD progress? 2) Does cholinesterase inhibitor therapy improves cognitive symptoms and daily activity of life (ADL) in SVD? 3) Is there any clinical difference among the subtypes of SVD? METHODS: According to cholinesterase inhibitor medications, patients with SVD were retrospectively analyzed using Hyoja Dementia registry. In this study, effects of treatment were assessed by comparing the scores of Korea version Mini-Mental State Examination (MMSE), Clinical Dementia Rating scale (CDR), Functional Independence Measure (FIM) at the base line with those at endpoints. RESULTS: After 12 months, the mean MMSE, CDR, FIM scores improved significantly in the cholinesterase inhibitor treatment group, compared with that in no-treatment group. In no-treatment group, annual decline of MMSE was 2.7, compared with 0.3 increment in the treatment group. White matter type of SVD showed worst prognosis compared with other types. CONCLUSIONS: This study suggests that SVD has more benign clinical course than previously reported, and cholinesterase inhibitor improves cognitive and ADL functions in SVD. Among the subtypes of SVD, the white matter type may have poor prognosis.
Activities of Daily Living ; Cholinesterases ; Dementia ; Dementia, Vascular ; Deoxycytidine ; Glycosaminoglycans ; Humans ; Korea ; Neurobehavioral Manifestations ; Prognosis ; Retrospective Studies

BACKGROUND: Reactive Oxygen Species (ROS) have been implicated in the pathophysiology of brain injury after ischemia/reperfusion. Recently, it has been reported that endonuclease G (EndoG), a mitochondrial protein, is activated by neuronal excitotoxicity and translocated into nucleus inducing apoptosis. However, it is not elucidated whether ROS are involved in the nuclear translocation of EndoG in focal cerebral ischemia/reperfusion in mice. We investigated whether treatment of manganese tetrakis (4-benzoic acid) porphyrin (MnTBAP) protects against early nuclear translocation of EndoG and reduces cerebral infarction after ischemia/reperfusion in mice METHODS: Adult male mice were subjected to middle cerebral artery occlusion (MCAO) for 60 min, followed by reperfusion. Immunohistochemistry and Western blot analysis for EndoG were performed at various time points after ischemia/reperfusion. Double staining with EndoG and Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end-labeling (TUNEL) was also performed. MnTBAP was used to determine whether the production of ROS could inhibit translocation of EndoG into the nucleus. RESULTS: Western blot analysis and Immunohistochemistry of EndoG showed that nuclear EndoG was detected as early as 4 hrs after reperfusion, and mitochondrial EndoG was significantly reduced at the same time. Double staining with EndoG and TUNEL showed a spatial relationship between EndoG expression and DNA fragmentation. MnTBAP-treated mice showed that the translocation of EndoG was attenuated in comparison with the vehicle- treated mice and decreased infarction volume after ischemia/reperfusion. CONCLUSIONS: MnTBAP reduced the generation of ROS, and inhibited the early translocation of EndoG, which was followed by the reduction of infarction volume in the ischemic brain after ischemia/reperfusion.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Brain ; Brain Injuries ; Cerebral Infarction* ; DNA Fragmentation ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Infarction ; Infarction, Middle Cerebral Artery ; Male ; Manganese ; Mice* ; Mitochondrial Proteins ; Neurons ; Reactive Oxygen Species ; Reperfusion ; Uridine Triphosphate

PURPOSE: Despite current acceptance of its neuroprotective property, whether the minocycline affords neuroprotection or how it protects neurons against seizures in the animal model of epilepsy is not clear. This prompts us to investigate whether minocycline is neuroprotective against kainic acid (KA)-induced seizure in mice through inhibition of caspase-dependent mitochondrial apoptotic pathways. METHODS: Adult male ICR mice were subjected to seizures by intrahippocampal KA injection with treatment of vehicle or minocycline. For cell death analysis, histological analysis using cresyl-violet staining, TdT-mediated dUTP-biotin nick end labeling (TUNEL), and histone-associated DNA fragmentation analysis were performed. Evaluation of cytochrome c, cleaved caspase-3, and caspase-3 activity were also performed. RESULTS: Hippocampal neuronal death was evident by cresyl violet staining, TUNEL, and cell death assay in vehicle-treated mice after KA injection; however, there was significant reduction of cell death in the minocycline-treated group. Significant decrease of both cytosolic translocation of cytochrome c and subsequent activation of caspase-3 after treatment of minocycline were demonstrated by Western blot analysis, immunohistochemical staining, and caspase-3 activity assay. CONCLUSION: This study suggests that minocycline may be neuroprotective against hippocampal damage after KA-induced seizure through inhibition of caspase-dependent cell death pathways.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Death* ; Cytochromes c ; Cytosol ; DNA Fragmentation ; Epilepsy ; Humans ; In Situ Nick-End Labeling ; Kainic Acid ; Male ; Mice* ; Mice, Inbred ICR ; Minocycline* ; Models, Animal ; Neurons ; Seizures* ; Viola

PURPOSE: Matrix metalloproteinases (MMPs) have been known to participate in various pathologic situations by modulating extracellular matrix. Although MMP-9 upregulation has been reported in some experimental seizure models, the exact role of MMP-9 in hippocampal cell death during epileptogenesis and subsequent mossy fiber sprouting (MFS) is not clear. Here, we investigated the role of MMP-9 on hippocampal cell death and MFS after pilocarpine-induced status epilepticus (SE) in mice, using highly specific hydroxamic MMP-9 inhibitor. METHODS: SE was induced by intraperitoneal pilocarpine administration in adult male C57BL/6 mice. MMP-9 specific inhibitor was administered intracerebroventrically 3 h after pilocarpine-induced SE. Expression and activation of MMP-9 were assessed by zymography and Western blot analysis. TdT-mediated UTP-biotin nick end labeling (TUNEL) and caspase-3 activity assay were also performed. MFS was investigated using Timm staining. RESULTS: Increased expression and activation of MMP-9 after pilocarpine-induced SE were observed in zymography and Western blot analysis. MMP-9 specific inhibitor decreased MMP-9 activity in in situ zymography and hippocampal cell death in cresyl violet staining. DNA fragmentation and caspase-3 activity were also attenuated by MMP-9 specific inhibitor. Four months after pilocarpine-induced SE, MFS was evident in vehicle-treated mice; in contrast, MFS was barely observed in MMP-9 specific inhibitor-treated mice. CONCLUSIONS: This study suggests MMP-9 is associated with hippocampal cell death and MFS after pilocarpine-induced SE. Furthermore, the findings that MMP-9 specific inhibitor ameliorates cell death and MFS offers the possibility of MMP-9 specific hydroxamic inhibitor as novel therapeutic strategy to reduce hippocampal damage and epileptogenesis.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Death* ; DNA Fragmentation ; Extracellular Matrix ; Humans ; Male ; Matrix Metalloproteinase 9 ; Matrix Metalloproteinases ; Mice* ; Mossy Fibers, Hippocampal ; Neurons* ; Pilocarpine ; Seizures ; Status Epilepticus* ; Up-Regulation ; Viola