No abstract available.
Dermoscopy ; Hemangioma* ; Lasers, Dye

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

No abstract available.
Cryptococcosis*

Primary intimal sarcoma of the pulmonary artery is a rare disease and there has been no report of any case originating from the pulmonary valve. Recently we experienced a 62 year-old female patient who had a primary intimal sarcoma of the pulmonary valve with distal metastasis. She was brought to medical attention due to exertional dyspnea facial edema productive coughing and general weakness for 1 month. Chest CT and echocardi-ography suggest an acute pulmonary thromboembolism or tumor. Exploration showed a large polypoid mass arising from the pulmonary leaflets and multiple masses on distal pulmonary arteries. We replaced the pulmonary valve and reconstructed the pulmonary artery. She received radiotherapy 1 month postoperatively and now 4 months after surgery she has begun receiving chemotherapy.
Cough ; Drug Therapy ; Dyspnea ; Edema ; Female ; Humans ; Middle Aged ; Neoplasm Metastasis ; Pulmonary Artery ; Pulmonary Embolism ; Pulmonary Valve* ; Radiotherapy ; Rare Diseases ; Sarcoma* ; Tomography, X-Ray Computed

No abstract available.
Neurilemmoma*

Myocarditis is defined as the myocardial inflammation caused by various infectious agents (such as virus, rickettsia , bacteria, protozoa, fungus and parasites). The clinical manifestations of myocarditis ranges from the asymptomatic state due to focal inflammation to fulminant fatal congestive heart failure secondary to diffuse myocardial involvement. Clinically, in some cases, it may simulate an acute myocardial infarction. We experienced a case of acute fulminant myocarditis that presented as acute myocardial infarction initially, and then progressed into and recovered from congestive heart failure and multiorgan failure.
Asymptomatic Diseases ; Bacteria ; Estrogens, Conjugated (USP)* ; Fungi ; Heart Failure* ; Inflammation ; Myocardial Infarction ; Myocarditis* ; Rickettsia