Child ; Child Health Services ; Humans ; Pediatrics ; Research

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

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

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.

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

OBJECTIVEThis study examined the expressions of plasma stromal cell derived factor-1 (SDF-1) and CXCR4 mRNA in peripheral blood mononuclear cells (PBMC) of children with Kawasaki disease (KD) and aimed to explore the significance of SDF-1 and CXCR4 mRNA in KD.

METHODSFifty-six children with KD (12 cases complicated by coronary artery lesions) and 60 age and gender-matched healthy children (normal controls) were enrolled in this study. Plasma SDF-1 levels and CXCR4 mRNA expression in PBMC were measured using ELISA and real-time quantitative PCR at the acute and convalescence stages of KD.

RESULTSPlasma SDF-1 levels (1833 +/- 395 ng/L vs 1126 +/- 408 ng/L; P < 0.05) and the CXCR4 mRNA expression in PBMC (6.57 +/- 2.81 vs 2.58 +/- 1.01; P < 0.01) in KD patients were significantly higher than those in normal controls at the acute stage. Both plasma SDF-1 levels and CXCR4 mRNA expression in KD patients decreased significantly at the convalescence stage, but nevertheless remained higher than those in the normal controls. The patients with concomitant coronary artery lesions showed higher CXCR4 mRNA levels than without at the acute stage (8.19 +/- 2.39 vs 6.13 +/- 2.77; P < 0.05).

CONCLUSIONSPlasma SDF-1 concentration and CXCR4 mRNA expression in PBMC increased in KD patients. CXCR4 mRNA might be involved in the development of coronary artery lesions in KD.

Chemokine CXCL12 ; Chemokines, CXC ; blood ; Child, Preschool ; Female ; Humans ; Infant ; Leukocytes, Mononuclear ; metabolism ; Male ; Mucocutaneous Lymph Node Syndrome ; blood ; RNA, Messenger ; blood ; Receptors, CXCR4 ; 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