Water matrix effect on UV photodegradation of perfluorooctanoic acid.

The widespread detection of perfluorinated compounds (PFCs) in the water environment has been a concern for the last several years, while effluents from wastewater treatment facilities are the major sources of these compounds. Even advanced oxidation technologies (AOTs) are not useful for mineralization of the compounds due to their very high stability. Photochemical techniques using particularly vacuum UV (VUV) have been found to be very promising in this regard. But the use of VUV in UV-based AOTs has still not progressed much. Moreover, the impact of water quality on PFCs photomineralization is unknown. This investigation aimed to assess photomineralization potentials of perfluorooctanoic acid (PFOA) in ultrapure water (UPW), tap water (TW), surface water and treated wastewater effluent using a reactor setup enabling maximum utilization of VUV emission of low pressure lamp in laboratory batch experiments. Neya River water (NRW) and the Nakahama Wastewater Treatment Plant Effluent (NWWTPE) represented surface water and treated wastewater effluent respectively. Also, tests were carried out in 50% diluted NRW and NWWTPE. PFOA photomineralization in terms of PFOA removal, defluorination and total organic carbon (TOC) removal are discussed. The usefulness of the method for PFOA mineralization in organic-rich wastewaters, and further research needs are also highlighted.

Thyrotropin-releasing hormone: role in the treatment of West syndrome and related epileptic encephalopathies.

Thyrotropin-releasing hormone (TRH) has been successfully used for treating children with neurologic disorders including epilepsy. The effectiveness of TRH and a TRH analog has been reported in West syndrome, Lennox-Gastaut syndrome, and early infantile epileptic encephalopathy that were intractable to anticonvulsants and adrenocorticotrophic hormone (ACTH). However, the peptide has not been widely studied as a treatment of intractable epilepsy outside Japan. TRH is safe in children and effective in some cases of West syndrome and Lennox-Gastaut syndrome. TRH is considered as a possible new strategy for treating West syndrome and Lennox-Gastaut syndrome prior to ACTH therapy, especially for the patient with an infection, immunosuppression, or severe organic lesions in the brain. The mechanisms of its antiepileptic action may differ from those of other antiepileptic drugs. One possibility is that TRH may act as an antiepileptic through a kynurenine mechanism, considering that kynurenic acid acts as an antagonist on the N-methyl-D-aspartate receptor complex.

Neuronal apoptosis mediated by IL-1 beta expression in viral encephalitis caused by a neuroadapted strain of the mumps virus (Kilham Strain) in hamsters.

The neuroadapted Kilham strain of the mumps virus produces lethal encephalitis in newborn hamsters after intracerebral inoculation. The pathogenesis of this encephalitis is not fully understood, but recently, apoptosis and associated cytokine production have been recognized to be major pathologic mechanisms by which viruses cause injury to neuronal host cells. To analyze the main factors producing brain injury in this viral encephalitis, the following questions were investigated: (1) does the virus induce neuronal apoptosis and (2) does expression of cytokines regulate the induction of neuronal apoptosis? Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) was used as a marker of neuronal apoptosis and TUNEL-positive neurons were widespread in the infected cerebral cortex. DNA fragmentation yielding DNA ladders characteristic of apoptosis was also observed in infected hamster brain tissue. Apoptotic cells in infected brains were observed after the appearance of inflammatory changes. Overexpression of IL-1 beta, but not TNF-alpha or Fas-L, was clearly detected in infected brains, as determined by Western blot and RT-PCR. Immunohistochemistry revealed a striking correlation between IL-1 beta expression and neuronal apoptosis. Injection of recombinant IL-1 beta into normal hamster brain resulted in neuronal apoptosis in cerebral cortex. On the other hand, neutralizing IL-1 beta antibodies decreased the number of cells undergoing apoptosis in infected hamster brains and subsequent death. We conclude that the fatal encephalitis induced by the Kilham strain of the mumps virus is mediated by immunopathological processes and that overexpression of IL-1 beta, which mediates the induction of neuronal apoptosis, may play a major role in these processes.

Experimental schizencephaly induced by Kilham strain of mumps virus: pathogenesis of cleft formation.

The pathogenesis of cleft formation in schizencephaly was analyzed by examining the brain lesions produced by the infection of the Kilham strain of mumps virus during the period of neuronal migration in hamsters. Mumps virus antigen was detected in the neuroepithelial cells within the ventricular zone, the choroid plexus in the lateral ventricles, and vimentin-immunoreactive radial glial fibers. The main pathological findings were cerebral hemorrhage, neuronal necrosis, microsulci on the cerebral cortex and cleft formation through the entire thickness of the cerebral mantle. The clefts seen in these experiments were lined by embryonal elements such as neuroepithelial cells and germinal cells. Based on these results and the original definition by Yakovlev and Wadsworth, the following two conclusions were suggested. First, the mumps virus localized to the neuroepithelial cells within the ventricular zone and the radial glial fibers may induce a destructive process and subsequent anomalous neuronal migration, resulting in cleft formation. Second, the formation of the ventricular cleft extending to the pial surface, which should be complete before the cortical infolding appears, is necessary in order to produce the characteristic cleft in schizencephaly which is associated with the pial-ependymal seam.

Experimental mumps virus-induced hydrocephalus: viral neurotropism and neuronal maturity.

In order to elucidate the relationship between virus neurotropism and neuronal maturity, two experiments were performed. First, mumps virus infectivity was compared among the different developmental stages of hamster brains inoculated with mumps virus by examining the immunohistochemical distribution of mumps virus antigen. Second, brain lesions resulting from mumps virus infection during the period of neuronal migration were histologically and ultrastructurally analyzed. Three groups of Syrian hamsters, Group E12 (fetuses on the 12th day of gestation), and Groups P2 and P30 (2 and 30 days old, respectively), were injected with mumps virus intraplacentally or intracerebrally. In Group P30, mumps virus antigen was observed specifically in ependymal cells and the choroid plexus. In addition to these areas, in Group P2, some neurons in layers II and III of the cerebral cortex also showed virus antigen immunoreactivity. In Group E12, mumps virus antigen accumulated primarily in the neuroepithelial cells within the ventricular zone. Neither specific intranuclear changes related to viral replication nor the formation of complete virions and nucleocapsids was observed. We conclude that mumps virus neurotropism to hamster brains is dependent on the degree of neuronal maturity and that mumps virus can induce an abortive infection and resultant neuronal cell necrosis in the immature developing hamster brain.

An unusual autopsy case of a victim stabbed during sadomasochistic prostitution.

A 29-year-old male who lived alone was found dead with his back leaning against the wall of his room. He had been stabbed in his abdomen with a survival-type knife. The victim's mouth was plugged with a pink-colored glove and was sealed with packing tape. His wrists were tightly tied behind his back with the same type of packing tape. The cause of death was diagnosed as hemorrhage from the right common iliac artery and vein. Due to the strange circumstances of the crime scene, the police initially considered the possibility of homicide by a group of assassins. Two months later, the police arrested a male suspect who was a member of a vice racketeer. The victim was characterized as a masochist and bisexual. He often hired the male suspect to perform sadomasochistic activities. On the day of the crime, the victim prepared a survival-type knife and packing tape himself to experience fear and pain more strongly. The victim hoped to use the knife to increase sexual excitement. In this case of sadomasochistic prostitution leading to death, the legal issues of homicide for money, malicious request of injury by the victim and accidental death were involved.

Partial coexistence of neuropeptide Y and calbindin D28k in the trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve in the rat.

Immunohistochemistry was applied to examine the correlation between neuropeptide Y (NPY) and the two calcium binding proteins (CaBPs) parvalbumin (PV) and calbindin D28k (CB) in the trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve (IAN) in the rat. Five days following transection and application of FluoroGold (FG) to the cut end of the IAN, approximately 14.8% (80/539) and 18.6% (90/483) of FG-labeled IAN neurons in the trigeminal ganglion showed PV-like immunoreactivity (-LI) and CB-LI, respectively. The mean +/- S.D. area of FG-labeled PV-like immunoreactive (-IR) cells (FG/PV-IR cells) and FG/CB-IR cells were 835.9 +/- 303.1 mu m2 and 712.7 +/- 246.0 mu m2, respectively. FG/PV-IR cells were significantly larger than FG/CB-IR cells. Fourteen days following peripheral axotomy of the IAN, NPY-LI appeared in the medium- to large-sized cells. Double immunostaining revealed that approximately 3.3% (52/1569) of NPY-IR cells in the axotomized trigeminal ganglion displayed PV-LI, while approximately 26.7% (371/1392) of NPY-IR cells displayed CB-LI. The mean +/- S.D. cross-sectional areas of PV-IR and CB-IR trigeminal ganglion cells displaying NPY-LI were 819.5 +/- 265.6 mu m2 and 766.5 +/- 279.7 mu m2, respectively. There were no significant differences in the cross-sectional areas either between NPY/PV-IR cells and NPY/CB-IR cells, or between FG/PV-IR cells and NPY/PV-IR cells, or between FG/CB-IR cells and NPY/CB-IR cells. The present results indicate that injury-evoked medium- to large-sized NPY neurons were a different population from large-sized PV neurons, and NPY was partly co-localized with CB.

Effects of sympathectomy on the cutaneous temperature abnormalities in rats with chronic constriction injury of the sciatic nerve.

Effects of surgical sympathectomy on the cutaneous temperature abnormalities of plantar surface evoked by the chronic constriction injury (CCI) of the sciatic nerve were investigated in the rat. In normal animals, there were very small temperature differences between both plantar surfaces. There were also very small temperature differences in plantar surfaces following the sympathectomy prior to CCI. In rats with CCI, the cutaneous temperature of the nerve-injured plantar surface was significantly higher (warmer) than that of the contralateral plantar surface during the first week following CCI, and then became lower (cooler). Surgical sympathectomy prior to and just after CCI significant suppressed the temperature abnormalities during the first week, but no effect was observed after 2 weeks following CCI. These observations indicate that sympathetic vasoconstriction may contribute to the cutaneous temperature abnormalities evoked by CCI during the early stage, but does not affect the abnormalities at later stages.

Cell size-specific appearance of neuropeptide Y in the trigeminal ganglion following peripheral axotomy of different branches of the mandibular nerve of the rat.

The effect of peripheral axotomy of the mental nerve (MN) and the cutaneous branch of the mylohyoid nerve (MhN) on the appearance of neuropeptide Y-like immunoreactivity (NPY-IR) in cells in the trigeminal ganglion of the rat was examined with combined retrograde-tracing and immunohistochemistry. Retrograde-tracing with True Blue (TB) revealed that the cell-size spectrum of the trigeminal cells sending peripheral processes to the MN (TB MN cells) ranged from 75.9 to 1560.5 microns2 (or from 9.8 to 44.6 microns in diameter); approximately 53% of TB MN cells were 300-600 microns2. TB MhN cells ranged from 47.7 to 1261.5 microns2 (or from 7.8 to 40.1 microns in diameter); 56% of TB MhN cells were < 300 microns2. In the normal trigeminal ganglion, there were no NPY-IR cells. 14 days after MN transection, approximately 35% of TB MN cells displayed NPY-IR. The distribution of the cross-sectional areas of NPY-IR cells after MN transection was very similar to that of TB MN cells. Transection of MhN also induced the appearance of NPY-IR in the trigeminal ganglion but to a lesser extent (approximately 17% of TB MhN cells). The distribution of the cross-sectional areas of NPY-IR cells after MhN transection was similar to that of NPY-IR cells after MN transection. These results indicate that injury-evoked NPY-IR is specific for the medium- and large-sized ganglion cells.