Standard auditory oddball ERPs are not sensitive enough to detect and/or quantify subtle objective neuropsychological changes in selected MTBI patients, especially those with traumatic MRI brain lesions. More complex auditory or other oddball paradigms have to be tested in the future.

Background: The aim of our study was to assess the role of laser polarimetry and visual evoked potentials (VEP) as potential biomarkers of disease progression in multiple sclerosis (MS).Participants: A total of 41 patients with MS (82 eyes) and 22 age-related healthy volunteers (44 eyes) completed the study. MS patients were divided into two groups, one (ON) with a history of optic neuritis (17 patients, 34 eyes) and another group (NON) without it (24 patients, 48 eyes). The MS patients and controls underwent laser polarimetry (GDx) examination of the retinal nerve fiber layer (RNFL). In the MS group, we also examined: Kurtzke “expanded disability status scale” (EDSS), the duration of the disorder, VEP – latency and amplitude, and conventional brain magnetic resonance imaging (MRI). Our results were statistically analyzed using ANOVA, Mann–Whitney, and Spearman correlation analyses.Results: In the MS group, brain atrophy and new T2 brain lesions in MRI correlated with both VEP latencies and amplitudes. Separate comparisons revealed VEP latency testing to be less sensitive in ON than in NON-patients. In ON patients, VEP amplitudes correlated mildly with brain atrophy (r = −0.15) and strongly with brain new MRI lesions (r = −0.8). In NON-patients, highly significant correlation of new MRI brain lesions with VEP latencies (r = 0.63, r = 0.6) and amplitudes (r = −0.3, r = −4.2) was found. EDSS also correlated with brain atrophy in this group (r = 0.5). Our study did not find a correlation of GDx measures with MRI tests. The GDx method was not able to detect whole brain demyelinization and the degeneration process, but was only able to reveal the involvement of optic nerves in ON and NON-patients.Conclusion: In our study, we found that both methods (VEP and GDx) can be used for the detection of optic nerve damage, but VEP was found to be superior in evaluating whole brain demyelinization and axonal degeneration. Both VEP and MRI, but not GDx, have an important role in monitoring disease progression in MS patients, independent of the ON history.

This study describes the karyotype of strain 270 of the yeast-like fungus Endomyces magnusii. It consists of 13 chromosomal DNA molecules, the size of which range between 1.2 and 5.7Mb producing a genome size of approximately 38Mb. By comparing the karyotype of six strains of E. magnusii, we revealed two main chromosome length polymorphisms (CLPs) associated with a pronounced difference in the total genome size (roughly 50%). Karyotype heterogeneity between two main CLPs was demonstrated by Southern analysis with three heterologous probes. The same species affiliation of six E. magnusii strains was confirmed by morphological and cytological studies, protein fingerprint comparisons, as well as restriction analysis of mitochondrial DNA and genomic Southern analysis.

SummaryHamster cells transformed with the Schmidt-l%uppin strain of avian sarcoma virus were selected for resistance to 5-bromodeoxyuridine (BUDI%). The resistant cell lines Ha(SR)BU-25 and Ha(SR)BU-100, proliferated in the presence of 25 and 100 ~g/ml BUDR, respectively. The resistant cells were deficient in thymidine kinase activity. They did not grow in HATG medium and did not incorporate labelled thymidine into DNA.Several single-cell clones were isolated in medium containing i00 ~g/ml BUDR from Ha(St~)BU-100 cells. These isolated cell clones differed in morphology and modal number of chromosomes from each other. None of the clones incorporated thymidine into DNA.The BUDR resistant cells were tested for their tumorigenicity in young hamsters. The number of cells needed for induction of tumor growth was higher with the BUDR resistant cells than with original clone of Ha(SR) cells.All clones of thymidine kinase deficient cells were tested for the presence of the virus genome by fusion with chicken embryo ceils. All clones of Ha(SR)BU-100 cells contained the virus genom% and infectious virus could be rescued from these cells.Therefore, the genome of avian sarcoma virus can persist in virogenic hamster cells growing in the presence of 5-bromodeo~yuridine. These virogenic cells deficient in thymidine kinase activity are useful for preparation of cell hybrids.

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The avian sarcoma virus genome (Schmidt-Ruppin strain) in transformed hamster cells resistant to 8-azaquanine [Ha(SR)AG-50] was strongly suppressed. The suppression was genetically stable and could not be overcome by attempts at induction with 5-iodo-2'-deoxyuridine. Fusion of hamster cells, which had suppressed virus genome, with chicken Rous-associated virus (RAV-1)-preinfected cells easily rescued the sarcoma virus. The rescued virus had envelope properties of RAV-1, as determined by viral interference, virus neutralization, and plating on genetically resistant chicken cells. By repeatedly cloning the rescued virus, we determined that virus recombined in the rescue experiment and that the recombinant virus had the envelope properties of helper virus used for its rescue. Cells with suppressed avian sarcoma virus genome were suitable for preparation of different recombinant viruses.

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