Hypnic headache is a unique headache disorder that occurs exclusively during sleep and often with "alarm-clock" consistency. It is a rare, benign, moderately severe, enduring headache syndrome that occurs in middle-aged to elderly adults and affects both sexes. The pathophysiology of hypnic headache is unknown, but its circardian periodicity and responsiveness to lithium suggest chronobiologic sleep disturbance contributing to the genesis of hypnic headache. We have recently experienced 2 cases of hypnic headache. They showed the characteristic signs of hypnic headache. We present our cases and discuss the pathophysiology of hypnic headache.
Adult ; Aged ; Headache Disorders ; Headache Disorders, Primary* ; Humans ; Lithium ; Periodicity

Influenza virus culture was performed in 149 patients with influenza-like illness who were admitted or visited to the Department of Pediatrics, Asan Medical Center from january, 1991 to March, 1991. The results were as follows; 1) Of the 149 patients, influenza virus were isolated in the 15 cases. 15 isolates were characterized by the WHO Collaborating Center for influenza: 7 cases were very similar to influenza A/Taiwan/1/86 (H1N1), 1 case was A/Beijing/353/89 (H3N2), 7 cases were B/Guangdon-g/55/89. 2) The age of 15 patients who were confirmed by viral isolation was between 11 months to 10 years. 3) The most common clinical symptoms were fever, vomiting, cough, nausea in deceasing order. 4) Of the total 149 patients, Reye syndrome occured in two patients and myositis occured in one: Influenza A/Taiwan/1/86 (H1N1) virus was isolated in one Reye syndrome patient.
Chungcheongnam-do ; Cough ; Fever ; Humans ; Influenza, Human* ; Myositis ; Nausea ; Orthomyxoviridae ; Pediatrics ; Reye Syndrome ; Seoul* ; Vomiting

No abstract available.
Education* ; Humans ; Licensure* ; Physical Therapists*

Recent studies have documented that Janus-activated kinase (JAK)-signal transducer and activator of transcription (STAT) pathway can modulate the apoptotic program in a myocardial ischemia/reperfusion (I/R) model. To date, however, limited studies have examined the role of JAK3 on myocardial I/R injury. Here, we investigated the potential effects of pharmacological JAK3 inhibition with JANEX-1 in a myocardial I/R model. Mice were subjected to 45 min of ischemia followed by varying periods of reperfusion. JANEX-1 was injected 1 h before ischemia by intraperitoneal injection. Treatment with JANEX-1 significantly decreased plasma creatine kinase and lactate dehydrogenase activities, reduced infarct size, reversed I/R-induced functional deterioration of the myocardium and reduced myocardial apoptosis. Histological analysis revealed an increase in neutrophil and macrophage infiltration within the infarcted area, which was markedly reduced by JANEX-1 treatment. In parallel, in in vitro studies where neutrophils and macrophages were treated with JANEX-1 or isolated from JAK3 knockout mice, there was an impairment in the migration potential toward interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), respectively. Of note, however, JANEX-1 did not affect the expression of IL-8 and MCP-1 in the myocardium. The pharmacological inhibition of JAK3 might represent an effective approach to reduce inflammation-mediated apoptotic damage initiated by myocardial I/R injury.
Animals ; Apoptosis/drug effects ; Cell Movement/drug effects ; Chemokines/pharmacology ; Heart Function Tests/drug effects ; Inflammation/pathology ; Janus Kinase 3/*antagonists & inhibitors/metabolism ; Macrophages/drug effects/metabolism/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Reperfusion Injury/drug therapy/*enzymology/physiopathology/*prevention & control ; Myocardium/enzymology/pathology ; Myocytes, Cardiac/drug effects/metabolism/pathology ; Neutrophils/drug effects/metabolism/pathology ; Quinazolines/pharmacology/therapeutic use