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Rabbits were immunized with herpes simplex and visna virus in complete Freund's adjuvant. Uv-inactivated herpes virus and the purified visna virus protein p 25 injected intraocularly into these rabbits elicited a moderate inflammatory cell infiltration in the epiretinal myelinated nerve fiber bundles accompanied by signs of demyelination. It is therefore apparent that also viral antigen can induce myelin lesions as a socalled “bystander effect” of a cell-mediated immune response (bystander demyelination).

The association between human cytomegalovirus (HCMV) infection and glioblastoma has been a source of debate in recent years because of conflicting laboratory reports concerning the presence of the virus in glioma tissue. HCMV is a ubiquitous herpesvirus that exhibits tropism for glial cells and has been shown to transform cells in vitro. Using sensitive immunohistochemical and in situ hybridization methods in 50 glioma samples, we detected HCMV antigen and DNA in 21/21 cases of glioblastoma, 9/12 cases of anaplastic gliomas and 14/17 cases of low-grade gliomas. Reactivity against the HCMV IE1 antigen (72 kDa) exhibited histology-specific patterns with more nuclear staining for anaplastic and low-grade gliomas, while GBMs showed nuclear and cytoplasmic staining that likely occurs with latent infection. Using IHC, the number of HCMV-positive cells in GBMs was 79% compared to 48% in lower grade tumors. Non-tumor areas of the tissue contained only four and 1% of HCMV-positive cells for GBMs and lower grade tumors, respectively. Hybridization to HCMV DNA in infected cells corresponded to patterns of immunoreactivity. Our findings support previous reports of the presence of HCMV infection in glioma tissues and advocate optimization of laboratory methods for the detection of active HCMV infections. This will allow for detection of low-level latent infections that may play an important role in the initiation and/or promotion of malignant gliomas.

The incorporationin vivo of14C-glycine into proteins has been studied during the period before and after the onset of neurotoxicity caused by an organic mercury compound and byp-bromophenylacetylurea in rats. The observations of Yoshinoet al. (1966) on the former intoxication have been confirmed in that an impairment of glycine incorporation into proteins was present in spinal ganglion cells, and may also be taking place in other tissues, before nerve fibre degeneration takes place. A similar reduction in amino acid incorporation into proteins during the period before the onset of paralysis due top-bromophenylacetylurea is found in spinal ganglia; this finding is confirmed by anin vitro method using14C-leucine as protein precursor.

The ultrastructure of the nerve cell change in swayback is presented. Notable features are an increase in cell size, progressive loss of Nissl substance, alteration in form and distribution of the Golgi apparatus and a striking increase in neurofibrils within the perikaryon. Similarities and differences in the fine structural changes of other pathological states are discussed.

Deposits similar to corpora amylacea were observed by electron microscopy within myelinated axons in the peripheral nerves in a case of familial spastic paralysis. Ultrastructurally the deposits consisted of randomly interlacing short filaments which were closely related to glycogen granules present in the periphery of the deposits. A possible relationship between the filamentous structures and glycogen granules is discussed. The significance of this inclusion and of related bodies is also discussed.

A non-productive syncytiogenic measles virus isolated from the brain of an SSPE patients was grown on Vero cells. The ultrastructure of the infected syncytia was studied by electron microscopic and immunoperoxidase techniques. It was compared with the isolate of the virus after passage in ferrets, the Edmonston strain of wild measles virus and the Halle productive strain of SSPE, all on Vero cells. The immunoperoxidase labeling of the cell membranes of the Edmonston measles virus infected cells was very heavy and uniform. In contrast, the labeling of the non-productive SSPE infected cells was clearly discontinuous. In the latter, there was a preponderance of intranuclear over cytoplasmic nucleocapsid formation, whereas cytoplasmic nucleocapsids were prevalent in the virion-producing strains. Many similarities between Vero cells infected with the wild measles virus and the Halle strain of SSPE were observed, although differences between this SSPE strain and strains reported by others were noted.

The aim of the work presented is to ascertain two points: 1. Whether filling of the ventricles stops or at least limits the production of cerebrospinal fluid by the choroid plexus; and 2. whether sudden removal of the fluid or its considerable limitation has an injurious influence on the central nervous system. The investigation was carried out on 25 adult mongrel dogs of both sexes, and 3 puppies. Agar, vaseline and silicon were used as filling material. 8 dogs (out of the 28 with filled ventricles) developed hydrocephalus. 17 dogs (out of the remaining 20) did not show any clinical (test punctures) or post-mortem trace of cerebrospinal fluid in the ventricular system. Three dogs showed cerebro-spinal fluid in the ventricles in addition to silicon or agar. The author's answer to the above points is the following: The author suggests that filling of the ventricles could be applied in treating human hydrocephalus.

Rare, generally pediatric oligodendroglioma-like neoplasms with extensive leptomeningeal dissemination have been interpreted variably as glial, oligodendroglial or glioneuronal. The clinicopathologic features have not been fully characterized. We studied 36 patients, 12 females and 24 males with a median age of 5 years (range 5 months–46 years). MRI demonstrated leptomeningeal enhancement, frequently with cystic or nodular T2 hyperintense lesions within the spinal cord/brain along the subpial surface. A discrete intraparenchymal lesion, usually in the spinal cord, was found in 25 (of 31) (81 %). Tumors contained oligodendroglioma-like cells with low-mitotic activity (median 0 per 10 high power fields, range 0–4), and rare ganglion/ganglioid cells in 6 cases (17 %). Tumors were mostly low-grade, with anaplastic progression in 8 (22 %). Immunohistochemistry demonstrated strong reactivity for OLIG2 (7 of 9) (78 %), and moderate/strong S100 (11 of 12) (92 %), GFAP (12 of 31) (39 %) and synaptophysin (19 of 27) (70 %). NeuN, EMA, and mutant IDH1 (R132H) protein were negative. Median MIB1 labeling index was 1.5 % (range <1–30 %). FISH (n = 13) or SNP array (n = 2) demonstrated 1p loss/intact 19q in 8 (53 %), 1p19q co-deletion in 3 (20 %), and no 1p or 19q loss in 4 (27 %). Clinical follow-up (n = 24) generally showed periods of stability or slow progression, but a subset of tumors progressed to anaplasia and behaved more aggressively. Nine patients (38 %) died 3 months–21 years after diagnosis (median total follow-up 5 years). We report a series of a neoplasm with distinct clinicopathologic and molecular features. Although most progress slowly, a significant fraction develop aggressive features.