All mate choice data_Dryad

Raw data on male and hermaphrodite choice experiments

Are Reports of Randomized Controlled Trials Improving over Time? A Systematic Review of 284 Articles Published in High-Impact General and Specialized Medical Journals

<div><p>Background</p><p>Inadequate reporting undermines findings of randomized controlled trials (RCTs). This study assessed and compared articles published in high-impact general medical and specialized journals.</p><p>Methods</p><p>Reports of RCTs published in high-impact general and specialized medical journals were identified through a search of MEDLINE from January to March of 1995, 2000, 2005, and 2010. Articles that provided original data on adult patients diagnosed with chronic conditions were included in the study. Data on trial characteristics, reporting of allocation concealment, quality score, and the presence of a trial flow diagram were extracted independently by two reviewers, and discrepancies were resolved by consensus or independent adjudication. Descriptive statistics were used for quantitative variables. Comparisons between general medical and specialized journals, and trends over time were performed using Chi-square tests.</p><p>Results</p><p>Reports of 284 trials were analyzed. There was a significantly higher proportion of RCTs published with adequate reporting of allocation concealment (p = 0.003), presentation of a trial flow diagram (p<0.0001) and high quality scores (p = 0.038) over time. Trials published in general medical journals had higher quality scores than those in specialized journals (p = 0.001), reported adequate allocation concealment more often (p = 0.013), and presented a trial flow diagram more often (p<0.001).</p><p>Interpretation</p><p>We found significant improvements in reporting quality of RCTs published in high-impact factor journals over the last fifteen years. These improvements are likely attributed to concerted international efforts to improve reporting quality such as CONSORT. There is still much room for improvement, especially among specialized journals.</p></div

Report Characteristics by Type of Journal Over Time.

<p>Note: *denotes comparisons between all time points for variable in general medical journals; **denotes comparisons between all time points for variable in specialized journals</p

FGF20 initiates lateral compartment differentiation before E14.5.

<p>(A–H) Immunostaining of Myo7a in <i>Fgf20^βGal/+</i> and <i>Fgf20^βGal/βGal</i> cochlear explants treated with or without FGF9 and cultured for 5 d (schematic). Treatment of <i>Fgf20^βGal/+</i> explants with FGF9, either at E14.5 (B) or E15.5 (F), did not have any effect on hair cell number compared to untreated explants (A,E). Treatment of <i>Fgf20^βGal/βGal</i> explants with FGF9 at E14.5 resulted in increased numbers of hair cells and decreased gaps (arrows) between hair cell clusters (D) compared to untreated explants (C). Treatment of <i>Fgf20^βGal/+</i> or <i>Fgf20^βGal/βGal</i> explants with FGF9 at E15.5 did not affect hair cell number or the formation of gaps (arrows) lacking sensory cells (G, H). (I) Quantitation of the number of hair cells. The number of OHCs and total hair cells were rescued by treatment with FGF9 at E14.5 but not at E15.5. * <i>p</i><0.05. (J–M) Immunostaining for Prox1 in <i>Fgf20^βGal/+</i> and <i>Fgf20^βGal/βGal</i> explants treated with or without FGF9 at E14.5 and cultured for 5 d (schematic). Treatment of <i>Fgf20^βGal/+</i> explants with FGF9 did not affect supporting cell number (K) compared to untreated explants (J). Treatment of <i>Fgf20^βGal/βGal</i> explants with FGF9 at E14.5 resulted in increased numbers of supporting cells and decreased gaps between sensory cell clusters (M) compared to untreated explants (L). (N) Quantitation of numbers of supporting cells in explants. The number of supporting cells was partially rescued in <i>Fgf20^βGal/βGal</i> explants by treatment with FGF9 at E14.5.</p

Expression of <i>Fgf20</i> in the developing inner ear.

<p>(A) βGal staining of E10.5 embryos showing anterio-ventral expression of <i>Fgf20</i> in the otic vesicle (OV). (B,C) Co-labeling of βGal and Sox2 showing that at E11.5 (B), the <i>Fgf20</i> expression domain is within the Sox2 expressing sensory patch and at E14.5 (C), <i>Fgf20</i> expression overlaps with the Sox2 expressing sensory domain. (D) Staining for βGal and for p27 expression showing that at E14.5, <i>Fgf20</i> expression partially overlaps with the medial region of p27 expression in the cochlear sensory epithelium. (E) βGal staining at P0 showing <i>Fgf20^βGal</i> expression in all sensory domains of the inner ear, including the cochlea (co), utricle (ut), saccule (sac), and crista of the semicircular canals (pc, lc, ac). (F) Co-staining of βGal, phalloidin, and p75 (pillar cells, PC) in P0 cochlea showing low-level <i>Fgf20</i> expression in medial supporting cells (Deiters' cells, DC) and HeC (lower panels), moderate expression in PCs, and highest expression in the inner phallangial cells (IPhC). <i>Fgf20^βGal</i> appears to be excluded from hair cells (upper panels). Scale bar: 100 µm. D, dorsal; A, anterior; M, medial.</p

Flow Diagram of articles identified, screened, and included in analysis.

<p>Flow Diagram of articles identified, screened, and included in analysis.</p

Schematic model of sensory cell development in the organ of Corti.

<p>Diagram showing that FGF20 specifically functions to initiate lateral compartment development. The differential activity of FGF20 suggests that there may be separate progenitor cells for the medial and lateral cochlear compartments.</p

Report Characteristics by Type of Journal.

<p>Report Characteristics by Type of Journal.</p

Lack of FGF20 results in undifferentiated lateral compartment cells.

<p>(A) Co-immunostaining of E-Cadherin and Myo6 showing that E-Cadherin stains lateral compartment cells in <i>Fgf20^βGal/+</i> cochlea (A, upper). In <i>Fgf20^βGal/βGal</i> cochlea, E-Cadherin stains all lateral compartment cells including cells localized in the region between sensory patches (A, lower, arrow). (B) Co-immunostaining of Sox2 and phalloidin showing that Sox2 labels supporting cells in <i>Fgf20^βGal/+</i> cochlea (B, upper). In <i>Fgf20^βGal/βGal</i> cochlea, the region between patches was marked by strong Sox2 staining (B, lower, arrows). (C) Co-immunostaining of p27 and phalloidin showing that p27 stains supporting cells in <i>Fgf20^βGal/+</i>cochlea (C, upper). In <i>Fgf20^βGal/βGal</i> cochlea, the region between patches was marked by strong p27 staining (C, lower, arrows). (D) Co-immunostaining of Sox2 and Prox1 of <i>Fgf20^βGal/βGal</i> explants treated with or without FGF9. Without FGF9 treatment (left), Sox2+/Prox1− cells were localized in the region between sensory patches (arrows). Treatment of <i>Fgf20^βGal/βGal</i> explants with FGF9 induced Sox2+/Prox1− cells to express Prox1 (right).</p

sj-docx-1-aut-10.1177_13623613221143592 – Supplemental material for Mental health–related hospitalizations among adolescents and emerging adults with autism in the United States: A retrospective, cross-sectional analysis of national hospital discharge data

Supplemental material, sj-docx-1-aut-10.1177_13623613221143592 for Mental health–related hospitalizations among adolescents and emerging adults with autism in the United States: A retrospective, cross-sectional analysis of national hospital discharge data by Darcy Jones (DJ) McMaughan, Sara Imanpour, Abigail Mulcahy, Jennifer Jones and Michael M Criss in Autism</p