52 research outputs found
Boot Camp World Tour
Purpose: A review of the history and growth of Science Boot Camps (SBCs) for Librarians across North America.
Methods: A panel of SBC planners gathered at the Midwinter meeting of the American Library Association in Chicago, IL, on January 31 2015 to share information with science librarians from across the U.S. and Canada.
Results: While the financing, scheduling and number of attenders of SBCs vary, they share the same goals-- informal, inexpensive, regional opportunities for professional development and networking. All planners emphasized the value of SBCs, and noted the heaviest workload fell on the venue organizers.
Conclusions: SBCs provide effective and economical opportunities for professional development. The SBC concept is robust, somewhat scalable, and is suitable for non-science disciplines as well
A crossover randomised controlled trial of oral mandibular advancement devices for obstructive sleep apnoea-hypopnoea (TOMADO)
Rationale Mandibular advancement devices (MADs)
are used to treat obstructive sleep apnoea-hypopnoea
syndrome (OSAHS) but evidence is lacking regarding
their clinical and cost-effectiveness in less severe disease.
Objectives To compare clinical- and cost-effectiveness
of a range of MADs against no treatment in mild to
moderate OSAHS.
Measurements and methods This open-label,
randomised, controlled, crossover trial was undertaken at
a UK sleep centre. Adults with Apnoea-Hypopnoea Index
(AHI) 5–<30/h and Epworth Sleepiness Scale (ESS) score
≥9 underwent 6 weeks of treatment with three nonadjustable
MADs: self-moulded (SleepPro 1; SP1);
semi-bespoke (SleepPro 2; SP2); fully-bespoke MAD
(bMAD); and 4 weeks no treatment. Primary outcome
was AHI scored by a polysomnographer blinded to
treatment. Secondary outcomes included ESS, quality of
life, resource use and cost.
Main results 90 patients were randomised and 83
were analysed. All devices reduced AHI compared with
no treatment by 26% (95% CI 11% to 38%, p=0.001)
for SP1, 33% (95% CI 24% to 41%) for SP2 and 36%
(95% CI 24% to 45%, p<0.001) for bMAD. ESS was
1.51 (95% CI 0.73 to 2.29, p<0.001, SP1) to 2.37
(95% CI 1.53 to 3.22, p<0.001, bMAD) lower than no
treatment (p<0.001 for all). Compliance was lower for
SP1, which was the least preferred treatment at trial exit.
All devices were cost-effective compared with no
treatment at a ÂŁ20 000/quality-adjusted life year (QALY)
threshold. SP2 was the most cost-effective up to
ÂŁ39 800/QALY.
Conclusions Non-adjustable MADs achieve clinically
important improvements in mild to moderate OSAHS and
are cost-effective
Characterization of behavioral, signaling and cytokine alterations in a rat neurodevelopmental model for schizophrenia, and their reversal by the 5-HT₆ receptor antagonist SB-399885
Post-weaning social isolation of rats produces neuroanatomical, neurochemical and behavioral alterations resembling some core features of schizophrenia. This study examined the ability of the 5-HT₆ receptor antagonist SB-399885 to reverse isolation-induced cognitive deficits, then investigated alterations in hippocampal cell proliferation and hippocampal and frontal cortical expression of selected intracellular signaling molecules and cytokines. Male Lister-hooded rats (weaned on post-natal day 21-24 and housed individually or in groups of 3-4) received six i.p. injections of vehicle (1% Tween 80, 1 mL/kg) or SB-399885 (5 or 10 mg/kg) over a two week period starting 40 days post-weaning, on the days that locomotor activity, novel object discrimination (NOD), pre-pulse inhibition of acoustic startle and acquisition, retention and extinction of a conditioned freezing response (CFR) were assessed. Tissue was collected 24 h after the final injection for immunohistochemistry, reverse-phase protein microarray and western blotting. Isolation rearing impaired NOD and cue-mediated CFR, decreased cell proliferation within the dentate gyrus, and elevated hippocampal TNFα levels and Cdc42 expression. SB-399885 reversed the NOD deficit and partially normalized CFR and cell proliferation. These effects were accompanied by altered expression of several members of the c-Jun N-terminal Kinase (JNK) and p38 MAPK signaling pathways (including TAK1, MKK4 and STAT3). Although JNK and p38 themselves were unaltered at this time point hippocampal TAK1 expression and phosphorylation correlated with visual recognition memory in the NOD task. Continued use of this neurodevelopmental model could further elucidate the neurobiology of schizophrenia and aid assessment of novel therapies for drug-resistant cognitive symptoms
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