Antibiotic-induced severe neutropenia with multidrug-dependent antineutrophil antibodies developed in a child with Streptococcus pneumoniae infection.

Drug-induced neutropenia (DIN), particularly that in which antibiotic-dependent antineutrophil antibodies have been detected, is a rare disorder. We report the case of a child with pneumococcal pneumonia, who experienced severe neutropenia during various antibiotic treatments. We detected 4 kinds (cefotaxim, augmentin, vancomycin, and tobramycin) of antibiotic-dependent antineutrophil antibodies by using the mixed passive hemagglutination assay (MPHA) technique with this child.

Nicotine inhibits bFGF-induced neurite outgrowth through suppression of NO synthesis in H19-7 cells.

NO (Nitric oxide) has been known as a biological signaling molecule that can function as a beneficial agent in physiologically essential functions such as differentiation or neurotransmission. In this study, we elucidated how nicotine inhibits neuronal differentiation induced by the basic fibroblast growth factor (bFGF) in hippocampal cell line, H19-7 cells, because nicotine is one of the key neuroregulatory components. Treatment of H19-7 cells with bFGF increased NO production through upregulated iNOS/ nNOS expression, and also increased expressions of neuronal markers such as brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and Neuro-D. Pretreatment of the cells with nicotine decreased iNOS promoter activity as well as iNOS/nNOS expression induced by bFGF, resulting in decreased NO production. Nicotine also suppressed expressions of BDNF, NT3 and Neuro-D, resulting in decreased bFGF-induced neurite outgrowth. These results indicate that nicotine inhibits bFGF-induced neuronal differentiation in H19-7 cells through inhibition of NO formation by suppressing iNOS/nNOS expressions.

Urine leukotriene E and eosinophil cationic protein in nasopharyngeal aspiration from young wheezy children.

Respiratory syncytial virus (RSV) infection is a risk factor for the development of asthma. It is very hard to distinguish bronchiolitis with respiratory virus infection from allergic asthma at first wheezing attack in early childhood. To distinguish wheezing children with RSV bronchiolitis from asthmatic children, we measured leukotriene E(4)(LTE(4)) in urine and ECP in nasopharyngeal aspiration (NPA) at first day of admission with wheezing attack. Thirty-two non-atopic children younger than the age of 3 yr with RSV induced bronchiolitis, 35 atopic asthmatic children with/without respiratory viral infection, and 23 children who exhibited no evidence of atopy, asthma, or virus infections as controls were selected in this study. We measured urinary LTE(4) and ECP level in NPA from subjects. Urinary LTE(4) concentrations in children with asthma were significantly higher than urinary LTE(4) in bronchiolitis and in controls (240.8 +/- 129.8 vs. 162.8 +/- 73.9 vs. 85.1 +/- 31.6 pg/ml). Children with RSV infection demonstrated higher urinary LTE(4) levels compared to children without RSV infection among asthmatic children. ECP in NPA was significantly correlated with urinary LTE(4) (r = 0.57, p < 0.01) in children entered this study who had detectable levels for both LTE(4) and ECP. In summary, Urinary LTE(4) concentrations may be suggested to useful mediators for differential diagnosis of wheezy diseases in early childhood. RSV infection also is associated with synergizing LT biosynthesis and this study demonstrated ECP in NPA was significantly correlated with urinary LTE(4) and may suggest that cysteinyl leukotriene initiate the production of ECP in early childhood, which could contribute to the development of wheeze.