Kawasaki disease is a systemic vasculitis of unknown etiology, with clinical observations suggesting a substantial genetic contribution to disease susceptibility. We conducted a genome-wide association study and replication analysis in 2,173 individuals with Kawasaki disease and 9,383 controls from five independent sample collections. Two loci exceeded the formal threshold for genome-wide significance. The first locus is a functional polymorphism in the IgG receptor gene FCGR2A (encoding an H131R substitution) (rs1801274; P = 7.35 × 10(-11), odds ratio (OR) = 1.32), with the A allele (coding for histadine) conferring elevated disease risk. The second locus is at 19q13, (P = 2.51 × 10(-9), OR = 1.42 for the rs2233152 SNP near MIA and RAB4B; P = 1.68 × 10(-12), OR = 1.52 for rs28493229 in ITPKC), which confirms previous findings(1). The involvement of the FCGR2A locus may have implications for understanding immune activation in Kawasaki disease pathogenesis and the mechanism of response to intravenous immunoglobulin, the only proven therapy for this disease.

The authors compared pre-treatment and post-treatment characteristics of 206 prospectively enrolled patients with Kawasaki disease (KD) responsive to intravenous immunoglobulin (IVIG) with those of 23 (10% of total) IVIG non-responders. Demographic characteristics were similar in both groups. Compared to IVIG responders, non-responders had a longer total duration of fever and a higher incidence of coronary artery lesions. Prior to IVIG, non-responders had higher neutrophil differential and C-reactive protein, and lower cholesterol. 24 hours after the IVIG infusion, a total leucocyte count >13.1×10(9)/l, neutrophil differential >51% and total protein <72 g/l showed reasonable sensitivity (91%, 91% and 64%, respectively) and specificity (89%, 76% and 78%, respectively) as independent characteristics of non-response to IVIG. Laboratory parameters before and shortly after IVIG may reflect the severity of inflammation in KD patients and assist in informing further management.

Numerous evidences support the pathogenesis that M. pneumoniae pneumonia is associated with cell-mediated immune reaction. We report 2 cases of severe M. pneumoniae pneumonia in previously healthy sisters, who were both admitted during an epidemic of M.pneumoniae pneumonia. The elder sister, who was 16 years old, was admitted with M. pneumoniae pneumonia. She showed no response to treatment with clarithromycin and levofloxacin, and eventually progressed to severe ARDS, requiring mechanical ventilation. After treatment with hydrocortisone (200 mg/day), there were rapid improvements in clinical manifestations and chest radiographic findings. The younger sister, who was 14 years old, was admitted 10 days later, presenting with fever but no pneumonic lesions on chest radiograph. Just like her sister, the infection showed no response to clarithromycin. Fever persisted and pneumonic consolidation with mild pleural effusion was noticed in the left lower lobe on the 5th hospital-day. After treatment with oral prednisolone (1 mg/kg), she showed rapid defervescence and on the 8th hospital day, no pneumonic lesions were detectable on chest radiograph. Given the fact that the pathogenesis of pneumonia and extrapulmonary manifestations in M. pneumoniae infection is immune-mediated, an immunosuppressive therapy would be validated for selected patients with M. pneumoniae infections.

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Purpose: To investigate the anti-cancer effect of methyl alcohol extract of Enteromorpha linza (Linnaeus) J. Agardh (MEEL) in U937 human leukemia cells. Methods: Cytotoxicity was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium

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