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Background: The field's understanding of the association between sluggish cognitive tempo (SCT) and sleep is severely limited by the lack of multi-method and multi-informant research designs that move beyond global ratings, often focused on a limited number of sleep-related domains, such as daytime sleepiness. The current study begins to address these limitations by using actigraphy, daily sleep diary, and self- and parent-report global ratings of sleep in adolescents, a developmental period marked by changes in SCT, sleep, and circadian function. As SCT and sleep are also associated with ADHD symptoms, we tested these associations in a sample of adolescents with and without ADHD. Methods: Adolescents (N = 302; M age = 13.17 years, 44.7% female) with (n = 162) and without ADHD (n = 140) and parents completed global ratings of sleep and daytime sleepiness, and adolescents completed a measure of circadian preference. Adolescents also wore actigraphs for approximately two weeks, during which daily diaries were completed. Results: Above and beyond demographic characteristics (i.e., sex, race, and family income), pubertal development, medication use, and ADHD group status, adolescents' self-reported SCT symptoms were uniquely associated with shorter sleep duration and later sleep onset per both actigraphy and daily diary. SCT symptoms were also uniquely associated with longer sleep onset latency and poorer overall sleep (per daily diary), more sleep/wake problems and daytime sleepiness (per adolescent rating), more difficulties initiating and maintaining sleep (per parent rating), and later eveningness preference (per adolescent rating). Nearly all significant effects remained in sensitivity analyses controlling for adolescent- or parent-reported ADHD symptom dimensions. Conclusions: Findings provide the strongest evidence to date for SCT being uniquely linked to poorer sleep, greater daytime sleepiness, and a later evening circadian preference across subjective and objective measures. Longitudinal studies are needed to evaluate predictive and bidirectional associations.

Earlier research by Mullins and Kiley (2002) [Studies in higher education, 27(4), 369-386] reported on the processes that experienced examiners go through when they assess research theses. Since that study two further studies have been undertaken, interviews with novice Australian examiners, reported here, and the analysis of approximately 100 examiners' reports (Kiley, 2004). These studies now allow us to address the comment made by many of the experienced examiners who were interviewed that it was not wise to send a research thesis, particularly one which is not strong, to inexperienced examiners. We also wanted to determine the extent to which less experienced examiners follow the same processes and use the same criteria as their more experienced colleagues, and whether there was any basis for the experienced examiners' comments. This paper draws particularly on the results of the interviews with 26 examiners and supervisors which indicated that by comparison with experienced examiners, less experienced examiners paid more attention to institutional criteria and the summative dimension of assessment; were unsure of the boundary conditions relating to very good or poor theses; and were more likely to refer back to their own postgraduate experience when reflecting on their approach to both supervision and examination. ng to very good or poor theses; and were more likely to refer back to their own postgraduate experience when reflecting on their approach to both supervision and examination.

Abstract: A 48-year-old woman with temporal lobe epilepsy and no prior history of psychiatric illness was started on topiramate (TPM). The dose was titrated up to 150 mg twice daily over 14 weeks and led to a significant reduction in seizure frequency. Upon reaching this dose, she developed intense pruritus and the firm belief that her skin was infected by parasites. She was diagnosed with delusional parasitosis (DP). Consequently, her TPM was weaned off and her DP settled completely without the use of antipsychotic medication. DP is characterized by the unshakeable conviction that small organisms infest the body despite the absence of confirmatory medical evidence. DP can occur in a wide variety of organic and psychiatric disorders or as an isolated delusional disorder. Rarely DP can be drug-induced. While psychiatric symptoms are a well recognized side-effect of TPM, this is, to our knowledge, the first reported case of TPM-induced DP. [Copyright &y& Elsevier]

The genome of Marburg virus (MBG), a filovirus, is 19.1 kb in length and thus the largest one found with negative-strand RNA viruses. The gene order - 3' untranslated region-NP-VP35-VP40-GP-VP30-VP24-L-5' untranslated region-resembles that of other non-segmented negative-strand (NNS) RNA viruses. Six species of polyadenylated subgenomic RNAs, isolated from MBG-infected cells, are complementary to the negative-strand RNA genome. They can be translated in vitro into the known structural proteins NP, GP (non-glycosylated form), VP40, VP35, VP30 and VP24. At the gene boundaries conserved transcriptional start (3'-NNCUNCNUNUAAUU-5') and stop signals (3'-UAAUUCUUUUU-5') are located containing the highly conserved pentamer 3'-UAAUU-5'. Comparison with other NNS RNA viruses shows conservation primarily in the termination signals, whereas the start signals are more variable. The intergenic regions vary in length and nucleotide composition. All genes have relatively long 3' and 5' end non-coding regions. The putative 3' and 5' leader RNA sequences of the MBG genome resemble those of other NNS RNA viruses in length, conservation at the 3' and 5' ends, and in being complementary at their extremities. The data support the concept of a common taxonomic order Mononegavirales comprising the Filoviridae, Paramyxoviridae, and Rhabdoviridae families.

The nucleotide sequence of the L gene of Marburg virus, strain Musoke, has been determined. The L gene has a single long open reading frame encoding a polypeptide of 2330 amino acids (MW 267,175) that represents the viral RNA-dependent RNA polymerase. The putative transcription start signal (3'CUACCUAUAAUU 5') and the termination signal (3' UAAUUCUUUUU 5') of the gene could be identified. Computer-assisted comparison of the L protein with L proteins of other nonsegmented negative-stranded RNA viruses (Paramyxoviridae: Sendai virus, Newcastle disease virus, human parainfluenza 3 virus, measles virus, human respiratory syncytial virus; Rhabdoviridae: vesicular stomatitis virus, rabies virus) revealed significant homologies primarily in the N-terminal half of the proteins. We have identified three common conserved boxes (A, B, and C) among filo-, paramyxo-, and rhabdovirus L proteins, which are probably involved in the polymerase function. The L proteins can be divided into an N-terminal half, which seems to accommodate the common enzymatic sites, and a C-terminal half carrying virus specific peculiarities. The data presented here suggest a common evolutionary history for all nonsegmented negative-stranded RNA viruses and show that filoviruses are more closely related to paramyxo- than to rhabdoviruses.

Polyacrylamide gel electrophoresis of purified Ebola virus revealed the presence of four major virion structural proteins which we have designated VP1, VP2, VP3 and VP4. Vesicular stomatitis virus (VSV) proteins were used as mol. wt. markers, and the virion proteins were found to have mol. wt. of 125000 (VP1), 104000 (VP2), 40000 (VP3) and 26000 (VP4). VP1 was labelled with glucosamine and is probably a glycoprotein. The density of the Ebola virion was approx. 1.14g/ml in potassium tartrate. Virus nucleocapsids with a density of 1.32g/ml in caesium chloride were released when virions were treated with detergents. Proteins VP2 and VP3 were consistently associated with released nucleocapsids and are probably the major structural nucleocapsid proteins analogous to the N protein of VSV. Protein VP4 was reduced or absent in released nucleocapsids and is probably analogous to the membrane (M) protein of VSV and similar viruses. The glycoprotein (VP1) is larger than the glycoprotein of any known negative-strand RNA virus and is not labelled well with 35S-methionine. VP1 is solubilized by detergent treatment, suggesting that it is a component of the virion spikes and analogous to the G protein of VSV. Our results, in conjunction with analysis of Ebola virion RNA (Regnery et al. 1980), strongly suggest that the virus is a negative-strand RNA virus and, along with marburg virus, may constitute a new taxon within this group.

Six messenger RNA species of Ebola virus were identified in infected Vero E6 cells. Virion RNA hybridizes to each of the mRNAs, confirming that Ebola virus possesses a negative-stranded RNA genome. The mRNAs are monocristronic transcripts, are synthesized in the presence of actinomycin D, and are polyadenylated. In vitro translation of mRNA preparations results in the synthesis of five authentic viral proteins and a putative unglycosylated form of the glycoprotein, demonstrated by immunoprecipitation with virus-specific antisera and SDS-PAGE. No mRNA species was detected for the polymerase (L protein) gene.

Korean haemorrhagic fever (KHF) (Hantaan virus), a rodent-borne viral illness, is an important cause of human disease throughout much of Asia and Eastern Europe. The agent responsible for KHF has not yet been conclusively identified. Plaque-purified KHF virus was concentrated and then banded in a potassium tartrate gradient. Material from the 1.17-1.19 g/ml band was examined by electron microscopy and particles with a morphology identical to that of the family Bunyaviridae were found. The particles were aggregated by KHF serum but not by saline solution or non-immune serum. Identification of KHF virus as a member of the family Bunyaviridae implies a potential for spread by arthropod vectors.

The plaque reduction neutralization test (PRNT) has been used routinely in serological studies with such arenaviruses as Junin, Machupo, and Parana. However, difficulties have been encountered in using the PRNT for LCM virus, while conflicting views have been expressed about the reliability and efficacy of the test with Lassa virus. We have therefore investigated and evaluated the plaque assay for Lassa virus. In addition, the suitability of the PRNT for determining the potency of a serum and its efficacy in passive immunization for the treatment of Lassa fever was also investigated. The Lassa virus plaque assay satisfied the criteria proposed by Cooper [1961] for determining satisfactory plaque technique. Lassa virus plaques appear within 3 days of inoculating Vero cell cultures. By day 5, the plaques are clearly defined, discrete, and measure 1.5 to 2.0 mm. In the plaque reduction neutralization test, the use of native non-inactivated serum was required for a reliable and reproducible determination of serum antibody titer. The potency and suitability of a serum for Lassa fever serotherapy was determined by the use of a constant serum-varying virus (CS-VV) and/or a constant virus-varying serum (CV-VS) PRN technique.

The 3' RNA base sequences of several Marburg (MBG) and Ebola (EBO) virus isolates have been determined. A comparison of these 3' terminal noncoding sequences with those of other negative strand RNA viruses suggests a unique phylogenic niche for Marburg and Ebola viruses. The translation initiation site and 35 N-terminal amino acids of the 3' proximal coding gene of a Zaire strain of Ebola virus was predicted. In addition, putative leader RNA sequences preceding the first gene are discussed in terms of possible regulatory functions.

Total RNA and small RNA species of several African arenavirus strains have been studied by T1-oligonucleotide mapping. Genetic heterogeneity is observed and discussed on the basis of evolutionary biology of the Lassa complex.

Genomic and messenger RNAs of a Zaire strain of Ebola virus were cloned, and inserts specific for the nucleoprotein gene were isolated and sequenced. The nucleoprotein gene is located proximal to the 3' end of the genome and is preceeded by a putative leader sequence. The gene begins with the transcriptional start site sequence 3'-UACUCCUUCUAAUU..., and ends with the polyadenylation site sequence 3'-... UAAUUCUUUUUU. The predicted coding region is 2217 bases in length and encodes a protein that contains 739 amino acids, with a calculated molecular weight of 83.3 kDa. The protein has an approximate net charge of -30 and can be divided into a hydrophobic N-terminal half and a hydrophilic and highly acidic C-terminal half. An in vitro transcript, generated from plasmid DNA containing the entire coding region, directs the synthesis of authentic nucleoprotein in a rabbit reticulocyte lysate system. The genomic organization and transcriptional signals of Ebola are similar to those of other nonsegmented, negative-strand RNA viruses, but nucleic acid or amino acid sequence comparisons indicate a lack of similarity.

The effect of cycloheximide on virus specific RNA synthesis in Vero cells infected with either wild-strain (Edmonston) or subacute sclerosing panencephalitis strain measles virus was investigated. At 3 days postinfection, cells treated with cycloheximide (2.6 x 10(-4) M) and then exposed to [(3)H]uridine showed a marked increase in labeled virus-specific RNA. A major portion of this incremental labeled RNA was putative viral mRNA which sedimented at 16, 22, and 30S. Five distinct classes of polyribosomes, which were not evident in untreated cells, were found in cycloheximide-treated cells and each contained similar species of virus-specific RNA. Viral nucleocapsid RNA, 50 and 18S, was synthesized and encapsidated in the presence of cycloheximide. The latter observation is in apparent contrast to reports that cycloheximide inhibits replication of RNA of classical paramyxoviruses, and may indicate that mechanisms for replicating RNA of measles virus are different from those for replicating RNA of paramyxoviruses.

Following two cases of Marburg virus disease in Kenya in 1980, viral haemorrhagic fever surveillance was undertaken in western Kenya. Over a 21-month period investigations, including virus isolation attempts, patient and contact serology, visits to areas where suspected cases occurred, interviewing family members and neighbours of suspected cases and following up any additional illnesses in these areas, were carried out. During the study two cases were found that were likely to have been Ebola haemorrhagic fever based on rising antibody titres or positive serology in contacts. Diagnoses of hepatitis A, hepatitis B, malaria, bacterial septicaemia or other causes were arrived at in 24 cases. No diagnosis could be made in 26 instances. 741 human sera were tested for antibodies against Marburg, Ebola, Congo haemorrhagic fever, Rift Valley fever or Lassa fever viruses by indirect fluorescence. Eight sera were positive for Ebola virus antibodies, all of which were from suspected cases or contacts of suspected cases. Two sera were antibody positive to Congo virus and one had antibodies against Rift Valley fever virus. No Marburg or Lassa virus antibodies were detected.