BACKGROUND: Two successive surveys were conducted in the same rural areas. The first survey was intended to obtain an initial estimate of public familiarity with, understanding of, and attitudes toward epilepsy. The second survey was performed to assess trends in public attitudes toward epilepsy and the putative effect of campaigns on such a trend. METHODS: Cross-sectional studies were conducted by means of a door-to-door interview using the same questionnaire, in which all residents over 19 years of age, living in the survey area, were targeted. Vehicles for the educational campaign took the form of lectures and small group discussions. RESULTS: Of 820 respondents in the first survey, 93% of respondents were familiar with epilepsy. Nevertheless, only 8.5% answered they had an epileptic person among their family or relatives. The understanding of epilepsy among respondents appeared to be not only based more on supernatural or superstitious thinking, but was also less comparable to that of other studies. The attitudes toward epilepsy also were far more negative in Korean rural areas than in other countries. The false belief that epilepsy cannot be treated was the factor that contributed most to negative attitudes in Korean rural areas. Even though it was not remarkable, and was not attributed to the campaigns entirely, a positive trend was obvious not only in understanding the cause of epilepsy but also in attitudes toward epilepsy. CONCLUSIONS: It is important to recognize the fact that the majority of respondents still remain unchanged in their misunderstanding of and negative attitudes toward epilepsy, regardless of the new positive trend. In order to ameliorate prejudices against epilepsy and allow epileptic persons to interact with and adapt to their surroundings properly, not only continuous and repetitive educational efforts but also the sympathy of professional and lay societies regarding epilepsy would be needed.
Cross-Sectional Studies ; Surveys and Questionnaires ; Education ; Epilepsy* ; Humans ; Jeollanam-do* ; Lectures ; Prejudice ; Recognition (Psychology) ; Thinking

OBJECTIVE: To compare the short-term effect and advantage of transforaminal epidural steroid injection (TFESI) performed using the Kambin's triangle and subpedicular approaches. METHOD: Forty-two patients with radicular pain from lumbar spinal stenosis were enrolled. Subjects were randomly assigned to one of two groups. All procedures were performed using C-arm KMC 950. The frequency of complications during the procedure and the effect of TFESI at 2 and 4 weeks after the procedure between the two groups were compared. Short-term outcomes were measured using a visual numeric scale (VNS) and a five-grade scale. Multiple logistic regression analyses were performed to evaluate the relationship between possible outcome predictors (Kambin's triangle or subpedicular approach, age, duration of symptoms and sex) and the therapeutic effect. RESULTS: VNS was improved 2 weeks after the injection and continued to improve until 4 weeks in both groups. There were no statistical differences in changes of VNS, effectiveness and contrast spread pattern between these two groups. No correlation was found between the other variables tested and therapeutic effect. Spinal nerve pricking occurred in five cases of the subpedicular and in none of the cases of the Kambin's triangle approach (p<0.05). CONCLUSION: The Kambin's triangle approach is as efficacious as the subpedicular approach for short-term effect and offers considerable advantages (i.e., less spinal nerve pricking during procedure). The Kambin's triangle approach maybe an alternative method for transforaminal epidural steroid injection in cases where needle tip positioning in the anterior epidural space is difficult.
Constriction, Pathologic ; Epidural Space ; Humans ; Imidazoles ; Injections, Epidural ; Logistic Models ; Needles ; Nitro Compounds ; Spinal Nerves ; Spinal Stenosis

Purpose: We studied the impact of arterial oxygen tension (PaO2) on the long term neurologic outcome in patients with acute carbon monoxide poisoning. Methods: The study population included 311 patients who presented to emergency department with acute CO poisoning from January 2015 to January 2018. These patients underwent arterial blood gas testing at the time of presentation. The baseline demographic, clinical, laboratory, and clinical outcome data were recorded. The primary outcome of interest was the long term neurologic status. Results: The normoxia group was significantly older and it had a higher incidence of diffusion weighted MRI abnormality, and this group needed multiple HBO sessions compared to the group with moderate or severe hyperoxia. Also, the incidence of altered mentality at discharge was higher in the normoxia group than that of the moderate hyperoxia group. The incidence of a poor long term neurologic outcome was 11.3%. The incidence of a poor long term neurologic outcome decreased as the PaO2 increased. The PaO2 was significantly lower in patients with a poor long term neurologic outcome than that of the patients with a good outcome 198 (165.2 to 231.1) mmHg in the good outcome group vs. 154 (119-162) mmHg in poor outcome, p<0.001). In multivariate logistic regression analysis, PaO2 was selected as an independent factor of the poor long-term neurologic outcome (OR 0.981 (95% CI: 0.968 to 0.995)) Conclusion Higher PaO2 was independently associated with a lower incidence of a poor long-term neurologic outcome.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Objective: Our study hypothesizes that the interaction between depression, alcohol intake, and smoking status can significantly influence the risk of acute coronary syndrome (ACS). We aim to investigate the magnitude of the association between depression and ACS risk and explore how alcohol intake and smoking status affect this association. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure of interest was the presence of depression, as measured using the Beck Depression Inventory score at baseline. The primary outcome was the occurrence of ACS observed in the biennial follow-up surveys. We used Cox proportional regression analysis to estimate the effect of depression on ACS incidence. We conducted interaction and joint effect analyses to explore the interactions between depression and health-related habits including alcohol intake and smoking with regard to ACS incidence. Results: During 16 years of follow-up among 3,254 individuals, we documented 88 cases of new-onset ACS (2.2 cases per 1,000 personyears). We found no association between depression and ACS risk; furthermore, the effect of depression on ACS risk by alcohol intake and smoking status did not differ significantly. In the analysis to observe the joint effect of smoking and depression, the multivariate hazard ratios of ACS were 1.26 (95% confidence interval [CI], 0.67–2.36) for non-smoking and depression, 1.52 (95% CI, 0.83–2.82) for smoking and non-depression, and 2.79 (95% CI, 1.21–6.41) for smoking and depression compared with non-smoking and non-depression. Conclusion Our study reveals the combined effect of depression and smoking on ACS risk, highlighting the potential benefits of concurrent interventions for both depression and smoking for cardiovascular health.

BACKGROUND: Brain natriuretic peptide (BNP) is expected to play a role in hemodynamic modulation. Its biologically inactive fragment, the 76-amino-acid N-terminal proBNP (NT-pro-BNP), was known as one of the biologic markers of congestive heart failure and other clinical situations. But, there are controversies about clinical significance of NT-pro-BNP in ischemic stroke. This study was performed to find the clinical significance of NT- pro-BNP in early stage of acute ischemic stroke. METHODS: NT-pro-BNP levels were measured in 610 consecutive patients who admitted to the department of neurology at Chonnam National University Hospital. 205 patients were excluded due to incomplete follow-up period (more than 2 weeks), systemic infection, and etc. 286 ischemic stroke patients and 119 patients as control subjects were enrolled. NT-pro-BNP levels between stroke group and control were analyzed. When the patients in stroke group had more than 300 pg/mL of NT-pro-BNP, they were regarded as high group and the others were low group. National Institute of Health Stroke Scale (NIHSS) was checked at admission and 2 weeks later. Relationship between changes of NIHSS and the NT-pro-BNP level was also investigated. RESULTS: The NT-pro-BNP levels were significantly increased in ischemic stroke patients (830.87 pg/mL) compared with control group (378.27 pg/mL) (p=0.002). And the high levels of NT-pro-BNP in stroke patients were related to severity on admission and cardioembolic infarction. But there was no correlation between NT-pro-BNP and improvement of NIHSS. CONCLUSIONS: In this study, significant relationship between the severity of ischemic stroke and NT-pro-BNP was found. But NT-pro-BNP was not related to early prognosis of ischemic stroke.
Biomarkers ; Follow-Up Studies ; Heart Failure ; Hemodynamics ; Humans ; Infarction ; Jeollanam-do ; Natriuretic Peptide, Brain ; Neurology ; Prognosis ; Stroke*