Photochemical decomposition of perfluorooctanoic acid mediated by iron in strongly acidic conditions.

The performance of a ferric ion mediated photochemical process for perfluorooctanoic acid (PFOA) decomposition in strongly acidic conditions of pH 2.0 was evaluated in comparison with those in weakly acidic conditions, pH 3.7 or pH 5.0, based on iron species composition and ferric ion regeneration. Complete decomposition of PFOA under UV irradiation was confirmed at pH 2.0, whereas perfluoroheptanoic acid (PFHpA) and other intermediates were accumulated in weakly acidic conditions. Iron states at each pH were evaluated using a chemical equilibrium model, Visual MINTEQ. The main iron species at pH 2.0 is Fe(3+) ion. Although Fe(3+) ion is consumed and is transformed to Fe(2+) ion by photochemical decomposition of PFOA and its intermediates, the produced Fe(2+) ion will change to Fe(3+) ion to restore chemical equilibrium. Continuous decomposition will occur at pH 2.0. However, half of the iron cannot be dissolved at pH 3.7. The main species of dissolved iron is Fe(OH)(2+). At pH 3.7 or higher pH, Fe(3+) ion will only be produced from the oxidation of Fe(2+) ion by hydroxyl radical produced by Fe(OH)(2+) under UV irradiation. These different mechanisms of Fe(3+) regeneration that prevail in strongly and weakly acidic conditions will engender different performances of the ferric ion.

Large congenital melanocytic nevi presenting with lissencephaly with an absent corpus callosum.

A neonatal case of provisional neurocutaneous melanosis presenting with lissencephaly is reported. Several congenital nevi were observed on the trunk and extremities of the infant, including a giant congenital hairy nevus over the skull. Brain magnetic resonance imaging revealed a marked ventricular dilatation with pachygyria and an absent corpus callosum; however, an injection of gadolinium did not demonstrate any enhanced lesions. Histopathological investigations by a brain biopsy showed a disorganized and anomalous embryonic cerebral architecture, suggesting lissencephaly. The detailed mechanism of this combined pathology is difficult to explain; however, a developmental disturbance was suggested to be present in both the neural crest cells and the neuroepithelial cells, resulting in the development of neurocutaneous melanosis accompanied with lissencephaly.

Neuronal apoptosis and gray matter heterotopia in microcephaly produced by cytosine arabinoside in mice.

Primary microcephaly can be accompanied by numerous migration anomalies. This experiment was undertaken to examine the pathogenesis of gray matter heterotopia and microcephaly that is produced after administering cytosine arabinoside (Ara-C) to mice. Pregnant mice were intraperitoneally injected with Ara-C at 30 mg/kg body weight on days 13.5 and 14.5 of gestation, and then their offspring were examined. On embryonic day 15.5, in the ventricular zone of the cingulate cortex, the neuroepithelial cells lacked BrdU immunoreactivity. Nestin-immunoreactive radial glial fibers and calretinin-positive subplate fibers were disrupted. TUNEL reaction was remarkable throughout the cerebral hemisphere. Subcortical heterotopia in the cingulate cortex and subependymal nodular heterotopia in the dorsolateral part of the lateral ventricles became detectable by the first day after birth. Thirty-two days after birth, microcephaly was apparent; subcortical heterotopia was observed to have increased in size while it was still located in the frontal and cingulate cortices. This experiment demonstrated that Ara-C induces neuronal apoptosis throughout the cerebral hemisphere. The immunohistochemical characteristics in the gray matter heterotopia suggest that both the subcortical and the subependymal heterotopias were formed by neurons originally committed to the neocortex. We conclude that the gray matter heterotopia that accompanies the microcephaly was produced by a disturbance of radial, tangential, and interkinetic neuronal migrations due to the toxicity of Ara-C in the immature developing brain.

The PDGF B-chain is involved in the ontogenic susceptibility of the developing rat brain to NMDA toxicity.

Hypoxic-ischemic (H-I) injury to neonatal brains can cause a life-long neuronal deficit because of increased susceptibility in the neonatal period. Excitotoxicity due to overstimulation of the N-methyl-d-aspartate receptor (NMDAR) is assumed to be the basis of the injury. However, the ontogenic profile of the susceptibility does not directly correlate with the levels of NMDAR expression. Platelet-derived growth factor B-chain (PDGF-B) has been reported to protect neurons by suppressing the NMDA-evoked current and translocating the glutamate transporter to the cell membrane. Thus, we assessed the relationship between the susceptibility to H-I injury and the expression of PDGF-B in neonatal rat brain. PDGF-B infusion before and after an intrastriatal NMDA injection significantly reduced the size of the lesions in 7-day-old rats, when they are most susceptible and the neuronal expression of PDGF-B is low. Fourteen-day-old neonatal rats were found to be resistant to NMDA injury, even though NMDARs are expressed at high levels in the brain at this age. Inhibition of PDGF-B protein synthesis by antisense oligodeoxynucleotides increased the size of the NMDA-induced lesions up to 6-fold at postnatal day 14, when PDGF-B is expressed at high levels in neurons. These data suggest that PDGF-B is an important physiological modulator of NMDAR excitability in the developing brain, and that the balance between the expression of NMDAR and PDGF-B partly determines the ontogenic susceptibility to brain injury. Enhancement of the PDGF-B/receptor signal pathway might rescue neonatal brains at risk of H-I injury.

Cytotoxic edema and interleukin-6 in hypertensive encephalopathy.

We report a female, 10 years of age, with juvenile rheumatoid arthritis accompanied by hypertensive encephalopathy. The patient developed a cytotoxic brain lesion, as revealed by the high signal intensity on diffusion-weighted magnetic resonance imaging, which corresponded to the hypoperfusion area on single-photon emission computed tomography scan using (99m)Tc-ethylcysteinatedimer. Cerebrospinal fluid interleukin-6 activity was elevated when the hypertensive encephalopathy revealed active central nervous system disease, and its activity decreased when the encephalopathy recovered from the central nervous system manifestations. We speculated that the cytotoxic edema and associated parenchymal damage in hypertensive encephalopathy were closely related to the intrathecal overproduction of interleukin-6.