Evidence-Based Medicine ; Humans ; Mucocutaneous Lymph Node Syndrome ; diagnosis ; therapy

Child ; Child Health Services ; Humans ; Pediatrics ; Research

Heart ; growth & development ; Humans ; MicroRNAs

Child ; Child Welfare ; Cooperative Behavior ; Humans ; Pediatrics ; education

Child ; Congresses as Topic ; Humans ; Pediatrics

Child ; Congresses as Topic ; Humans ; Pediatrics

Gata4 is an important transcription factor in heart development. Gata4 post-transcriptional protein modification regulates transcriptional activity and DNA binding, which in turn affects expression of downstream genes and transcription factors, differentiation of embryonic stem cells and cardiogenesis. This article summarizes the effect of post-transcriptional protein modification on transcriptional activity of Gata4 and the relationship between this effect and congenital heart disease. It was shown that acetylation, phosphorylation and SUMOylation upregulate transcriptional activity, DNA binding, downstream gene expression and embryonic stem cell differentiation. On the other hand, methylation and deacetylation downregulate Gata4 transcriptional activity. Post-transcriptional protein modification of Gata4 is very important in clinical research on congenital and other heart diseases.
Acetylation ; Animals ; GATA4 Transcription Factor ; chemistry ; genetics ; metabolism ; Humans ; Methylation ; Phosphorylation ; Protein Processing, Post-Translational ; Sumoylation

Objective To analyze the clinical, radiological, pathological and microbiological features of invasive pulmonary aspergillosis (IPA) to improve clinical management.Methods Retrospective analysis of 20 pathologically and/or microbiologically confirmed IPA cases in our hospital from January 2005 to August 2008. Results Group A (with underlying diseases) included 13 patients (underlying malignancy in 9 patients, including 5 cases of hematological malignancy, COPD in 2 patients, pulmonary tuberculosis and bronchiectasis in 1 each). Group B (without underlying disease) included 7 patients (2 patients with a long time of fluffy toy contact, another 1 had exposure to moldy rice, and 3 had exposure to polluted water). All these 20 patients had pulmonary invasion revealed by CT imaging. Multiple changes were identified in 16 patients. Bilateral pulmonary infiltrates and/or consolidation were revealed in 7 patients. Multiple nodules were seen in 9 patients. Four patients had solitary lesions, including isolated nodules in 2 patients and segment consolidation in the other 2 patients. Pulmonary cavity without fluid level was found in 8 patients (40.0%). Eighteen cases received antifungal therapy. The overall efficacy rate was 55.6%. The efficacy rate in group A and B was 45.5% and 5/7 respectively. The average time to symptomatic relief was (12.0±2.8) days. The time to lung lesion improvement on CT was (17.4±2.9) days. The time to significant CT improvement was (34.3±9.9) days. The time to the resolution of active lesion was (56.4±6.2) days.Conclusions IPA may occur in immunocompetent patients without underlying disease. Most IPA patients have bilateral multiple pulmonary nodules and cavities on CT. The time to the resolution of active pulmonary lesions is about 6 weeks.

OBJECTIVEKawasaki disease (KD) is a febrile illness of childhood. The etiology of KD remains unknown. Multiple theories exist, including an infectious etiology and an immunological abnormality. Cardiac involvement ranges from myocarditis and pericarditis in the acute stage to the development of coronary artery aneurysms later in the course. The present study aimed to explore the effect of monocyte chemotactic protein-1 (MCP-1) in Kawasaki disease and its relationship with damage to the coronary arteries during the development of KD.

METHODSPlasma MCP-1 concentrations were measured by enzyme-linked immunosorbent assay (ELISA), and MCP-1 mRNA expression in peripheral blood mononuclear cells (PBMC) was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in comparison of three groups: 56 patients with KD, 60 age-matched patients with non-infectious diseases, and 66 age-matched febrile patients with various diseases.

RESULTSPlasma MCP-1 concentration and MCP-1 mRNA expression in PBMC of patients with active KD [(409.55 +/- 97.42) pg/ml] and (1.97 +/- 0.77) were higher than those of control group. Plasma MCP-1 levels and MCP-1 mRNA expression of inactive KD group [(301.64 +/- 71.55) pg/ml] and (1.31 +/- 0.39) were significantly higher than those of non-infectious diseases patients. There was a marked increase in patients with inactive KD than those of non-infective patients, but there were no significant differences between inactive KD and febrile patients. Plasma MCP-1 levels and MCP-1 mRNA expression were markedly increased in KD patients with coronary artery lesions than those in patients without coronary artery lesions.

CONCLUSIONPlasma MCP-1 concentration and MCP-1 mRNA expression in PBMC were significantly increased in patients with KD, and they were higher in KD with coronary artery lesions. It indicates that MCP-1 may be a useful parameter for monitoring disease activity in patients with KD.

Chemokine CCL2 ; blood ; genetics ; metabolism ; Child ; Child, Preschool ; Coronary Vessels ; pathology ; Female ; Humans ; Infant ; Leukocytes, Mononuclear ; metabolism ; Male ; Mucocutaneous Lymph Node Syndrome ; blood ; genetics ; pathology ; RNA, Messenger ; genetics

OBJECTIVETo investigate the roles of nitric oxide (NO) and eNOS in the pathogenesis of vasovagal syncope (VVS).

METHODSFourteen children with VVS (group A), 10 children with syncope other than vasovagal (group B) and 20 healthy volunteers (group C) were enrolled. Plasma NO levels in groups A and B were determined before and at the termination of the head-up tilt table test (HUT). The G894T polymorphism within the eNOS gene was determined in the three groups.

RESULTSPlasma NO levels in group A increased significantly when syncope attacked from 76.7+/-9.6 micromol/L (before HUT) to 90.0+/-11.4 micromol/L (P<0.05). After the syncope attack was improved, plasma NO level in group A was significantly reduced. There were no statistical differences in plasma NO levels before and after the HUT in group B. Determining the G894T polymorphism within the eNOS gene showed that group A was associated with a higher incidence of the GT gene type as compared to groups B and C (42.9% vs 10%; P<0.05).

CONCLUSIONSPlasma NO may be involved in the pathogenesis of VVS. The increased plasma NO level may be associated with the G894T polymorphism of the eNOS gene.

Child ; Humans ; Nitric Oxide ; blood ; physiology ; Nitric Oxide Synthase Type III ; genetics ; physiology ; Polymorphism, Genetic ; Syncope, Vasovagal ; etiology