BACKGROUNDFunctional neuroimaging study has opened an avenue for exploring the pathophysiology of cluster headache (CH). The aim of our study was to assess the changes in brain activity in CH patients by the regional homogeneity method using resting-state functional magnetic resonance imaging technique.

METHODSThe functional magnetic resonance imaging scans were obtained for 12 male CH patients with spontaneous right-sided headache attacks during "in attack" and "out of attack" periods and 12 age- and sex-matched normal controls. The data were analyzed to detect the altered brain activity by the regional homogeneity method using statistical parametric mapping software.

RESULTSAltered regional homogeneity was detected in the anterior cingulate cortex, the posterior cingulate cortex, the prefrontal cortex, insular cortex, and other brain regions involved in pain processing and modulation among different groups.

CONCLUSIONIt is referred that these brain regions with altered regional homogeneity might be related to the pain processing and modulation of CH.

Adult ; Case-Control Studies ; Cluster Headache ; physiopathology ; Female ; Humans ; Magnetic Resonance Imaging ; methods ; Male ; Middle Aged ; Young Adult

OBJECTIVETo study the pulmonary pathology in patients died of fatal human influenza A(H1N1) infection.

METHODSEight cases of fatal human influenza A (H1N1) infection, including 2 autopsy cases and 6 paramortem needle puncture biopsies, were enrolled into the study. Histologic examination, immunohistochemitry, flow cytometry and Western blotting were carried out.

RESULTSThe major pathologic changes included necrotizing bronchiolitis with surrounding inflammation, diffuse alveolar damage and pulmonary hemorrhage. Influenza viral antigen expression was detected in the lung tissue by Western blotting. Immunohistochemical study demonstrated the presence of nuclear protein and hemagglutinin virus antigens in parts of trachea, bronchial epithelium and glands, alveolar epithelium, macrophages and endothelium. Flow cytometry showed that the apoptotic rate of type II pneumocytes (32.15%, 78.15%) was significantly higher than that of the controls (1.93%, 3.77%).

CONCLUSIONNecrotizing bronchiolitis, diffuse alveolar damage and pulmonary hemorrhage followed by pulmonary fibrosis in late stage are the major pathologic changes in fatal human influenza A (H1N1) infection.

Adolescent ; Adult ; Aged ; Alveolar Epithelial Cells ; pathology ; Antigens, Viral ; metabolism ; Apoptosis ; Autopsy ; Biopsy, Needle ; Bronchiolitis, Viral ; pathology ; Child ; Child, Preschool ; Female ; Hemagglutinin Glycoproteins, Influenza Virus ; metabolism ; Humans ; Influenza A Virus, H1N1 Subtype ; immunology ; Influenza, Human ; metabolism ; mortality ; pathology ; virology ; Lung ; immunology ; metabolism ; pathology ; Male ; Middle Aged ; Nuclear Proteins ; metabolism ; Pulmonary Alveoli ; pathology ; Pulmonary Fibrosis ; pathology ; Young Adult

OBJECTIVETo observe effect of Shufeng Xuanfei Recipe (SXR) and Jiebiao Qingli Recipe (JQR) on mRNA and protein expressions of Toll-like receptor 7 (TLR7), myeloid differentiation factor 88 (MyD88), and nuclear factor-kappaB (NF-kappaB) in mice infected with influenza virus FM1.

METHODSOne hundred and eight mice were randomly divided into nine groups, i.e., the normal control group, the model group, the Oseltamivir group (at the daily dose of 2.5 g/mL), the high dose SXR group (at the daily dose of 3.762 g/kg), the middle dose SXR group (at the daily dose of 1.881 g/kg), the low dose SXR group (at the daily dose of 0.941 g/kg), the high dose JQR group (at the daily dose of 4.368 g/kg), the middle dose JQR group (at the daily dose of 2.184 g/kg), and the low dose JQR group (at the daily dose of 1.092 g/kg), 12 in each group. All mice were mildly anesthetized by ether. Mice in the normal control group were treated by nasal drop of 0.05 mL normal saline, while mice in the rest groups were infected by nasal drop of 0.05 mL influenza virus strain FM1 (LD50). The successful modeling rate was 100%. All medication was performed by gastrogavage 2 h after infection. Distilled water was given by gastrogavage to mice in the normal control group and the model group at the daily dose of 0.2 mL, each time per day for 4 successive days. mRNA expressions of TLR7, MyD88, and NF-kappaB in the lung tissue were determined by Western blot.

RESULTSCompared with the normal control group, mRNA expressions of TLR7, MyD88, and NF-kappaB increased in the model group (P < 0.01). Compared with the model group, mRNA and protein expressions of TLR7, MyD88, and NF-kappaB decreased in the Oseltamivir group, the high, middle, and low dose SXR groups (P < 0.05, P < 0.01); mRNA and protein expressions of TLR7 and NF-kappaB decreased in the high and middle dose JQR groups (P < 0.05, P < 0.01); mRNA expressions of MyD88 decreased in the high and middle dose JQR groups (P < 0.05); protein expressions of MyD88 decreased in the middle dose JQR group (P < 0.05); protein expressions of TLR7 and NF-kappaB decreased in the low dose JQR group (P < 0.05). Compared with the Oseltamivir group, protein expressions of MyD88 decreased in the low dose SXR group (P < 0.05); protein expressions of NF-kappaB decreased in the middle and low dose SXR groups (P < 0.01); mRNA and protein expressions of TLR7 (P < 0.05, P < 0.01), and protein expressions of MyD88 (P < 0.01) decreased in the high, middle, and low dose JQR groups; mRNA and protein expressions of NF-kappaB decreased in the low dose JQR group (P < 0.05, P < 0.01).

CONCLUSIONSEach dose SXR and middle dose JQR could down-regulating the activity of NF-kappaB through adjusting MyD88 dependent TLR signal pathway, thus fighting against influenza virus. SXR was more effective than JQR.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Lung ; metabolism ; Male ; Membrane Glycoproteins ; genetics ; metabolism ; Mice ; Mice, Inbred ICR ; Myeloid Differentiation Factor 88 ; genetics ; metabolism ; NF-kappa B ; genetics ; metabolism ; Orthomyxoviridae ; Orthomyxoviridae Infections ; drug therapy ; metabolism ; Pneumonia, Viral ; drug therapy ; metabolism ; RNA, Messenger ; genetics ; Signal Transduction ; drug effects ; Toll-Like Receptor 7 ; genetics ; metabolism