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Prevalence of Vestibular Disorders in Moderate-Severe Traumatic Brain Injury (TBI) Scoping Review Search StrategyTo identify studies to include or consider for this scoping review, the review team worked with a librarian (BF) to develop detailed search strategies for each database. The PRISMA-ScR extension was followed for search reporting. The librarian (BF) developed the search for PubMed (NLM) and translated the search for every database searched. The PubMed (NLM) search strategy was reviewed by the research team to check for accuracy and term relevancy, and all final searches were peer-reviewed by another librarian (TN) following the PRESS checklist. The databases included in this search are PubMed (NLM), CINAHL (EbscoHost), and Embase (Elsevier), using a combination of keywords and subject headings. A grey literature search included Trip Pro Database, clinicaltrials.gov (Classic), and WHO International Clinical Trials. The search was limited to studies published since 1990 and a filter to exclude studies on children was used. All final searches were performed on November 8, 2023 by the librarian and were fully reported (BF). The search resulted in 7,472 studies 1,239 duplicate studies were found and omitted by the librarian using the EndNote 20 and following the Bramer et al. (2016) duplicate identification strategy. This resulted in 6,233 studies that were screened by title and abstract by two independent reviewers. If a tiebreaker was needed, a third reviewer was called in. This process was repeated for full text article screening and article selection.
Urinary Incontinence & Female Athletes Systematic Review Search StrategyTo identify studies to include or consider for this systematic review, the review team worked with a medical librarian (SB) to develop detailed search strategies for each database. The PRISMA-S extension was followed for search reporting. The medical librarian (SB) developed the search for PubMed (NLM) and translated the search for every database searched. The PubMed (NLM) search strategy was reviewed by the research team to check for accuracy and term relevancy, and all final searches were peer-reviewed by another medical librarian (JB) following the PRESS checklist. The databases included in this search are PubMed (NLM), Embase (Elsevier), Web of Science Core Collection (Clarivate Analytics), CINAHL (Ebscohost), SPORTDiscus (Ebscohost), Sports Medicine & Education Index (ProQuest), and Cochrane Central (Wiley) using a combination of keywords and subject headings. A grey literature search included Clinical Trials (https://classic.clinicaltrials.gov) and WHO International Clinical Trials Registry (https://trialsearch.who.int/) . All final searches were performed on November 1, 2023, by the librarian and were fully reported (SB). The full search strategies as reported by the librarian are provided in Appendix (___). A summary of the search results from databases: PubMed (NLM) from inception to 11/1/2023 (42 Results) Embase (Elsevier) from inception to 11/1/2023 (88 Results) Web of Science Core Collection (Clarivate Analytics) from inception to 11/1/2023 (35 Results) CINAHL (Ebscohost) from inception to 11/1/2023 (22 results) SPORTDiscus with Full Text (Ebscohost) from inception to 11/1/2023 (28 results) Sports Medicine & Education Index (ProQuest) from inception to 11/1/2023 (19 results) Cochrane Central (Wiley) from inception to 11/1/2023 (9 results) The search resulted in 270 studies and 92 duplicate studies were found and omitted by the librarian (SB) using the EndNote 20 duplicate identification strategy. This resulted in 178 records to screen from databases or registers. Studies were screened by title and abstract by two blinded and independent reviewers. If a tiebreaker was needed, a third reviewer was called in. This process was repeated for full text article screening and article selection.
Distinct segments within the enhancer region collaborate to specify the type of leukemia induced by nondefective Friend and Moloney virusesThe nondefective Moloney and Friend murine leukemia viruses induce T-cell lymphomas and erythroleukemias, respectively, after being injected into newborn NFS mice. In previous studies, we showed that the distinct disease specificities of the two viruses could be switched by exchanging a small segment, about 200 nucleotides in length, encompassing their enhancer regions. This segment included the direct repeat sequence and an adjacent GC-rich region of about 20 nucleotides defined in studies of Moloney murine sarcoma virus enhancer-promoter function (L. A. Laimins, P. Gruss, R. Pozzatti, and G. Khoury, J. Virol. 49:183-189, 1984). The direct repeats of Friend and Moloney viruses are identical in a central core sequence of 32 nucleotides but have sequence differences on either side of this core as well as in their GC-rich segments. To determine whether disease specificity resides in part or in all of the direct repeat and GC-rich region, we constructed recombinants between Friend and Moloney viruses within this segment and tested them for their disease-inducing phenotypes. We found that disease specificity, in particular the ability of Friend virus sequence to confer erythroleukemogenicity on Moloney virus, is encoded throughout the region in at least three separable segments: the 5' and 3' halves of the direct repeat and the GC-rich segment. When just one of these segments (either both 5' halves of the direct repeat, both 3' halves, or just the GC-rich segment) from Friend virus was substituted into a Moloney virus genome, it conferred only a negligible or low incidence of erythroleukemia (less than or equal to 5% to between 10 and 15%). Any two segments together were considerably more potent (35 to 95% erythroleukemia), with the most effective pair being the two halves of the direct repeat. Individual segments and pairs of segments were considerably more potent determinants when they were matched with a genome of the same origin. Thus, although sequences outside the enhancer region are minor determinants of disease specificity when the enhancer is derived entirely from either Friend or Moloney virus, they can play a significant role when the enhancer is of mixed origin. Some recombinant enhancers conferred a long latent period of disease induction. This was particularly striking when the 5' halves of each copy of the direct repeat sequence were derived from Moloney virus and the 3' halves were derived from Friend virus.(ABSTRACT TRUNCATED AT 400 WORDS)
Disease specificity of nondefective Friend and Moloney murine leukemia viruses is controlled by a small number of nucleotidesMoloney murine leukemia virus induces T cell lymphomas after injection into NFS mice, whereas the nondefective Friend virus induces erythroleukemias. Previous studies showed that sequences encompassing the viral transcriptional signals in U3 are the primary determinant of this phenotype in recombinants between these two viruses. To more precisely identify the sequences responsible, we constructed additional recombinants, within U3, between Friend and Moloney viruses and assayed these recombinants for for their disease specificity. We found that a fragment 191 bases long that included the direct repeat (enhancer) region plus 22 nucleotides to its 3' side from Friend virus was sufficient to convert Moloney virus to a virus that induced only erythroleukemias. A 171-base-long fragment of Moloney virus, including just the direct repeat, converted Friend virus to a virus that induced primarily lymphomas (about 85% of mice injected). We also constructed Moloney and Friend virus variants with one rather than two copies of the enhancer element. These viruses retained their disease specificity, although they exhibited a marked increase in the latent period of disease induction. Together the results suggest that 25 or fewer nucleotide differences, lying within and also just 3' of the direct repeat, are the primary determinant of the distinct disease specificities of nondefective Friend and Moloney viruses.
Alignment of U3 region sequences of mammalian type C viruses: identification of highly conserved motifs and implications for enhancer designWe aligned published sequences for the U3 region of 35 type C mammalian retroviruses. The alignment reveals that certain sequence motifs within the U3 region are strikingly conserved. A number of these motifs correspond to previously identified sites. In particular, we found that the enhancer region of most of the viruses examined contains a binding site for leukemia virus factor b, a viral corelike element, the consensus motif for nuclear factor 1, and the glucocorticoid response element. Most viruses containing more than one copy of enhancer sequences include these binding sites in both copies of the repeat. We consider this set of binding sites to constitute a framework for the enhancers of this set of viruses. Other highly conserved motifs in the U3 region include the retrovirus inverted repeat sequence, a negative regulatory element, and the CCAAT and TATA boxes. In addition, we identified two novel motifs in the promoter region that were exceptionally highly conserved but have not been previously described.