Reactive oxygen species are recognized as important mediators of biological responses. Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide. In several cell lines, oxidant stress has been linked to the activation of death programs. Here, we report for the first time that high ambient glucose concentration induces apoptosis in murine and human mesangial cells by an oxidant-dependent mechanism. The signaling cascade activated by glucose-induced oxidant stress included the heterodimeric redox-sensitive transcription factor NF-kappaB, which exhibited an upregulation in p65/c-Rel binding activity and suppressed binding activity of the p50 dimer. Recruitment of NF-kappaB and mesangial cell apoptosis were both inhibited by antioxidants, implicating oxidant-induced activation of NF-kappaB in the transmission of the death signal. The genetic program for glucose-induced mesangial cell apoptosis was characterized by an upregulation of the Bax/Bcl-2 ratio. In addition, phosphorylation of the proapoptotic protein Bad was attenuated in mesangial cells maintained at high-glucose concentration, favoring progression of the apoptotic process. These perturbations in the expression and phosphorylation of the Bcl-2 family were coupled with the release of cytochrome c from mitochondria and caspase activation. Our findings indicate that in mesangial cells exposed to high ambient glucose concentration, oxidant stress is a proximate event in the activation of the death program, which culminates in mitochondrial dysfunction and caspase-3 activation, as the terminal event.

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Eleven infants had echogenic stripes in the basal ganglia at the location of the lenticulostriate arteries, seen by head ultrasound. Eight patients had proven infection with rubella (2 patients), cytomegalovirus (2 patients), syphilis (1 patient) or bacterial meningitis (3 patients). Two had probable intrauterine infection clinically, but the organism could not be identified; one had trisomy 13. A recent report correlated these echogenic stripes in patients with viral and syphilitic intracranial infection with pathologically proven mineralizing vasculopathy. Our group manifests a wider range of intracerebral infection associated with this finding. Duplex sonography performed in four infants showed these stripes in vivo to be arteries in the basal ganglia. The lenticulostriate arteries are not normally visible by grey scale sonography but their Doppler signal may be elicited in normal children and they are rendered vividly visible by color Doppler. Echogenicity of these vessels is highly suggestive of intracranial infection because it is not encountered normally or in babies with non infectious intracranial disorders except trisomy 13. The prognostic significance of this finding is yet to be determined.

Background Inferior turbinectomy on patients of all ages is a controversial procedure. Its effect on children has been reported little in the literature and the few studies that are available involved relatively older children, i.e., >10 years old. Nasal obstruction caused by extensive hypertrophy of the inferior turbinates is not an uncommon observation in the pediatric population. The clinical manifestations might present as snoring, noisy breathing, mouth breathing, and, possibly, sleep apnea. Methods In this study, we followed 227 children >10 years of age who underwent inferior turbinectomy (27 children also underwent a revision of an earlier adenoidectomy), of whom 179 children had significant relief of nasal obstruction at the 1-year follow-up. Results Nocturnal breathing was reported to be more regular and otherwise improved in the 36 children with a suspected history of sleep apnea. Forty-two of 47 children who had thick nasal secretions and did not respond to antibiotic therapy before the operation had significant relief postoperatively. Postoperative complications were few and their number did not exceed that of adults. Conclusions A complete inferior turbinectomy should be considered in children >10 years of age who have hypertrophied inferior turbinates that cause major interference with nasal breathing.