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Objective. Our purpose is to describe the characteristics and the outcome of melamine-induced renal and urinary tract injury in young children who consumed melamine-contaminated infant formula. Methods. This is a descriptive longitudinal study over 2 years in 240 children with melamine-induced urolithiasis screened in our hospital from September 15 to October 31, 2008. Ultrasonography and serum creatinine (SCr), urea, β2-microglobulin (MG), cystatin C (Cys C), urinary Cr (UCr), microalbumin (mALB), α1-MG, β2-MG, n-acetyl-β-d-glucosaminidase (NAG) and retinol-binding protein (RBP) measurements were performed. Results. The children ranged in age from 1 to 82 months, and 145 were males. The largest calculus was 33 mm in diameter. X-ray diffraction pattern of the calculi displayed two diffraction peaks at 10.9° and 27.7° (2θ). Surgical management was performed in 14 patients. In 226 patients without surgical management, the calculi were passed in 59.63% patients within 1 month, in 85.40% within 6 and in 91.15% within 24 months. Increased SCr and urea levels were noted in three and six patients, respectively, at the time of diagnosis. The SCr, serum β2-MG, and Cys C levels at the time of diagnosis were higher than those at 3 and 6 months after diagnosis (P < 0.05, respectively). The levels of mALB/UCr, NAG/UCr, and RBP/UCr at the time of diagnosis were higher than those at 3, 6, 12, and 24 months after diagnosis (P < 0.05, respectively). α1-MG/UCr and β2-MG/UCr levels at the time of diagnosis were similar to those at 3 months after diagnosis, and significantly higher than those in the follow-up period (P < 0.05, respectively). Conclusion. Melamine might injure both the renal glomerulus and the tubule, and that the predominant lesion is urolithiasis. The compositions of melamine-induced urolithiasis are melamine and cyanuric acid crystals. The urolithiasis might persist for over 2 years and cause irreversible damage. Therefore, a long-term follow-up for all patients is required. [ABSTRACT FROM AUTHOR]

The aim is to investigate the spectrum of disease in 378 infants with human cytomegalovirus infection. In these patients, 27.78% were systemic infection and 72.22% involved single organ infection. Hepatitis, thrombocytopenic purpura, pneumonia were predominant with 33.07%, 13.49%, 6.35% respectively. The rate of HCMV systemic infection in infants younger than 2 weeks was higher than in those older than 2 weeks. The gB genotype analysis in 107 cases showed 53 gBI, 20 gBII, 18 gBIII, 7 gBI+gBII, 5 gBI+gBIII and 4 gBII+gBIII. These results suggest that HCMV can infect multiorgan and has varietal clinic feature. The gBI genotype is most prevalent. [ABSTRACT FROM AUTHOR]

The objective was to investigate the clinical features, glycoprotein B (gB) genotype and therapy of the human cytomegalovirus (CMV)-associated idiopathic thrombocytopenic purpura (ITP) in Chinese children. Clinical features and laboratory data of 25 CMV-associated ITP, including 18 males and 7 females with a median age of 0.3 y, were analysed and compared with 116 CMV-negative ITP. The CMV gB of 17 cases was genotyped. Apart from dermatorrhagia, jaundice was noted in 6 cases. Cough, diarrhoea, fever, splenohepatomegaly, alimentary tract haemorrhage and raised ALT were also found. Compared with CMV-negative ITP, CMV-associated ITP has a younger median age, raised ALT and AST, and longer hospitalization (p<0.05, respectively). The most prevalent genotype was gB1 (15/17), followed by coinfection and gB3. Compared with congenitally CMV-infected children in our previous study, more prevalence of gB1 was noted (40/79 vs 15/17, p=0.004). Most of these cases were receiving the therapy of immunoglobulin, corticoid and/or gancyclovir with good therapeutic effect except for 2 cases. In conclusion, CMV infection, especially gB1 genotype, is an important cause of ITP and careful examination of markers of CMV in all cases of apparent 'idiopathic' ITP is required. Combination therapy of immunoglobulin, corticoid and gancyclovir is effective. [ABSTRACT FROM AUTHOR]

Our objective was to investigate the role of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and their cellular sources in childhood asthma. We used 12 controls and 16 asthmatic children. The levels of MMP-9 and TIMP-1 in bronchoalveolar lavage (BAL) cells of asthmatic children were measured immunocytochemically. The positive level index, defined as the percentage of positive-stained cells × average optical density, was used to assess the expressing levels of MMP-9 and TIMP-1. The percentages of eosinophils and mast cells in bronchoalveolar lavage fluid (BALF) of asthmatic children were increased. Levels of MMP-9 and TIMP-1 in BAL cell of asthmatic children were increased significantly at about 30- and 35-fold relative to the controls, respectively. These results suggest that both MMP-9 and TIMP-1 contribute to tissue remodeling. MMP-9, which mediates the degradation of extracellular matrix (ECM), is increased significantly in the early or acute stage and may play a role in ECM degeneration. Excessive TIMP-1 may be synthesized following MMP-9 production when the body tries to repair the damage, which results in excessive deposition of ECM component. [ABSTRACT FROM AUTHOR]

Our objective was to investigate the role of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) and their cellular sources in guinea pig asthma model following ovalbumin (OA) challenge. Twenty guinea pigs were divided into 2 groups: OA-challenged group were sensitized by intraperitoneal injection with OA and exposed to OA while the control group used saline in a similar manner. The positive level index (PLI), defined as the percentage of positive-stained cells × average optical density, was used to assess the expressing levels of MMP-9 and TIMP-1. The levels of MMP-9 from OA-challenged group were significantly higher than those of controls. However, no significant difference of the TIMP-1 levels between the OA-challenged group and controls were found. MMP-9 was expressed strongly in both inflammatory and structural cells while TIMP-1 was expressed weakly in inflammatory cells and structural cells. Our results implied that MMP-9 may contribute to tissue remodeling in asthma and both structural and inflammatory cells within lung tissue are the main cellular sources of MMP-9. Excessive expression of MMP-9 m the early or acute stage of asthma may be associated with the initiation of bronchial injury and inflammatory cells accumulation. [ABSTRACT FROM AUTHOR]