Museum material reveals a frog parasite emergence after the invasion of the cane toad in Australia

<p>Abstract</p> <p>Background</p> <p>A parasite morphologically indistinguishable from <it>Myxidium immersum </it>(Myxozoa: Myxosporea) found in gallbladders of the invasive cane toad (<it>Bufo marinus</it>) was identified in Australian frogs. Because no written record exists for such a parasite in Australian endemic frogs in 19^thand early 20^thcentury, it was assumed that the cane toad introduced this parasite. While we cannot go back in time ourselves, we investigated whether material at the museum of natural history could be used to retrieve parasites, and whether they were infected at the time of their collection (specifically prior to and after the cane toad translocation to Australia in 1935).</p> <p>Results</p> <p>Using the herpetological collection at the Australian Museum we showed that no myxospores were found in any animals (<it>n </it>= 115) prior to the cane toad invasion (1879-1935). The green and golden bell frog (<it>Litoria aurea</it>), the Peron's tree frog (<it>Litoria peronii</it>), the green tree frog (<it>Litoria caerulea</it>) and the striped marsh frog (<it>Limnodynastes peronii</it>) were all negative for the presence of the parasite using microscopy of the gallbladder content and its histology. These results were sufficient to conclude that the population was free from this disease (at the expected minimum prevalence of 5%) at 99.7% confidence level using the 115 voucher specimens in the Australian Museum. Similarly, museum specimens (<it>n </it>= 29) of the green and golden bell frog from New Caledonia, where it was introduced in 19^thcentury, did not show the presence of myxospores. The earliest specimen positive for myxospores in a gallbladder was a green tree frog from 1966. Myxospores were found in eight (7.1%, <it>n </it>= 112) frogs in the post cane toad introduction period.</p> <p>Conclusion</p> <p>Australian wildlife is increasingly under threat, and amphibian decline is one of the most dramatic examples. The museum material proved essential to directly support the evidence of parasite emergence in Australian native frogs. This parasite can be considered one of the luckiest parasites, because it has found an empty niche in Australia. It now flourishes in > 20 endemic and exotic frog species, but its consequences are yet to be fully understood.</p

Hip and Groin Injuries in National Collegiate Athletic Association Women’s Soccer Players

Background: Hip and groin injuries are common in competitive soccer players and have been shown to be significant sources of time loss. There are few studies describing the epidemiology of hip and groin injuries in female National Collegiate Athletic Association (NCAA) soccer players. Purpose: To describe the epidemiology of hip and groin injuries in women's collegiate soccer players. Study Design: Descriptive epidemiology study. Methods: The NCAA Injury Surveillance System/Program (ISS/ISP) was analyzed from 2004 through 2014 for data related to hip and groin injuries in female collegiate soccer players. Injuries and athlete-exposures (AEs) were reported by athletic trainers. Data were stratified by time of season, event type, injury type, treatment outcome, time loss, and player field position. Results: Between 2004 and 2014, there were 439 recorded hip or groin injuries in female soccer players and an overall rate of injury of 0.57 per 1000 AEs. Injuries were 12.0 times more likely to occur during the preseason (4.41/1000 AEs) as opposed to during the regular season (0.37/1000 AEs) (injury rate ratio [IRR], 12.01; 95% confidence interval [CI], 9.92-14.55) or postseason (0.38/1000 AEs) (IRR, 11.55; 95% CI, 7.06-18.91). Rates of injury were similar during the regular season and postseason (IRR, 0.96; 95% CI, 0.59-1.58). Rates of injury were higher during competition (0.69/1000 AEs) than during practice (0.52/1000 AEs) (IRR, 1.33; 95% CI, 1.08-1.63). Most injuries were new (87.5%; n = 384) and unlikely to recur (12.5%; n = 55). Conclusion: Hip and groin injuries in female NCAA soccer players are uncommon, and fortunately, most players return to play quickly without recurrence. Future prospective studies should evaluate the effectiveness of strength and conditioning programs in preventing these injuries.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Lower Back Injuries in National Collegiate Athletic Association Football Players: A 5-Season Epidemiological Study

Background: Low back injuries are common in collegiate football players and can frequently lead to persistent pain, reinjuries, and time lost from participation. Purpose: To describe the epidemiology of back injuries in National Collegiate Athletic Association (NCAA) football players during the 2009/2010 through 2013/2014 academic years utilizing the NCAA Injury Surveillance Program (ISP) database. Study Design: Descriptive epidemiology study. Methods: A convenience sample of NCAA varsity football teams was utilized to determine the rates and patterns of back injuries as well as to generate national injury estimates. The rates and distribution of back injuries were identified within the context of mechanism of injury, injury chronicity, and time lost from sport. Injury rates were calculated as the number of injuries divided by the total number of athlete-exposures (AEs). Incidence rate ratios were calculated to compare the rates of injury between season, event type, mechanism of injury, injury chronicity, and time lost from sport. Results: Nationally, there were 267 low back injuries reported in the database. These were used to estimate 7076 back injuries over the 5-year period, approximately 82% of which were new injuries. The injuries occurred at a rate of 2.70 per 10,000 AEs. Overall, injuries were 3.12 times more likely to occur in competitions than in practices. Athletes were 4.67 times more likely to sustain a back injury during the preseason compared with the postseason but were 1.41 times more likely to sustain a low back injury during the preseason compared with the regular season. Both contact and noncontact were reported equally as the mechanism of injury (37.8% and 38.3%, respectively), and unspecified low back pain was the most common injury (64.2%). Only 1.6% of patients required surgery for their injury, and the majority of athletes (59.6%) returned to play within 24 hours. Conclusion: There was a relatively high rate of lumbar back injuries at the collegiate level (2.70/10,000 AEs), the majority of which were new injuries. About 18% of reported injuries were reinjuries. Although very few required surgery, a careful examination and work-up should be conducted to evaluate each injury. Regimented physical therapy and reconditioning programs are recommended to avert reinjuries.NCAAOpen access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Spectroscopy of the neighboring massive clusters Abell 222 and Abell 223

We present a spectroscopic catalog of the neighboring massive clusters Abell 222 and Abell 223. The catalog contains the positions, redshifts, R magnitudes, V-R color, as well as the equivalent widths for a number of lines for 183 galaxies, 153 of them belonging to the A 222 and A 223 system. We determine the heliocentric redshifts to be z=0.2126+/-0.0008 for A 222 and z=0.2079+/-0.0008 for A 223. The velocity dispersions of both clusters in the cluster restframe are about the same: sigma = 1014^{+90}_{-71} km/s and sigma = 1032^{+99}_{-76} km/s for A 222 and A 223, respectively. While we find evidence for substructure in the spatial distribution of A 223, no kinematic substructure can be detected. From the red cluster sequence identified in a color--magnitude--diagram we determine the luminosity of both clusters and derive mass--to--light ratios in the R--band of (M/L)_A222 = (202+/-43) h_70 M_{su}n/L_{sun} and (M/L)_A223 = (149+/-33) h_70 M_{sun}/L_{sun}. Additionally we identify a group of background galaxies at z ~ 0.242.Comment: Accepted for publication in A&A, 10 pages, 9 figures, full version of table 2 included in source distribution, version with higher quality images available from http://www.astro.uni-bonn.de/~dietrich

Patient-derived iPSC-cerebral organoid modeling of the 17q11.2 microdeletion syndrome establishes CRLF3 as a critical regulator of neurogenesis

Neurodevelopmental disorders are often caused by chromosomal microdeletions comprising numerous contiguous genes. A subset of neurofibromatosis type 1 (NF1) patients with severe developmental delays and intellectual disability harbors such a microdeletion event on chromosome 17q11.2, involving the NF1 gene and flanking regions (NF1 total gene deletion [NF1-TGD]). Using patient-derived human induced pluripotent stem cell (hiPSC)-forebrain cerebral organoids (hCOs), we identify both neural stem cell (NSC) proliferation and neuronal maturation abnormalities in NF1-TGD hCOs. While increased NSC proliferation results from decreased NF1/RAS regulation, the neuronal differentiation, survival, and maturation defects are caused by reduced cytokine receptor-like factor 3 (CRLF3) expression and impaired RhoA signaling. Furthermore, we demonstrate a higher autistic trait burden in NF1 patients harboring a deleterious germline mutation in the CRLF3 gene (c.1166T\u3eC, p.Leu389Pro). Collectively, these findings identify a causative gene within the NF1-TGD locus responsible for hCO neuronal abnormalities and autism in children with NF1

Human iPSC-derived neurons and cerebral organoids establish differential effects of germline NF1 gene mutations

Neurofibromatosis type 1 (NF1) is a common neurodevelopmental disorder caused by a spectrum of distinct germline NF1 gene mutations, traditionally viewed as equivalent loss-of-function alleles. To specifically address the issue of mutational equivalency in a disease with considerable clinical heterogeneity, we engineered seven isogenic human induced pluripotent stem cell lines, each with a different NF1 patient NF1 mutation, to identify potential differential effects of NF1 mutations on human central nervous system cells and tissues. Although all mutations increased proliferation and RAS activity in 2D neural progenitor cells (NPCs) and astrocytes, we observed striking differences between NF1 mutations on 2D NPC dopamine levels, and 3D NPC proliferation, apoptosis, and neuronal differentiation in developing cerebral organoids. Together, these findings demonstrate differential effects of NF1 gene mutations at the cellular and tissue levels, suggesting that the germline NF1 gene mutation is one factor that underlies clinical variability

Acute low back pain is marked by variability: An internet-based pilot study

<p>Abstract</p> <p>Background</p> <p>Pain variability in acute LBP has received limited study. The objectives of this pilot study were to characterize fluctuations in pain during acute LBP, to determine whether self-reported 'flares' of pain represent discrete periods of increased pain intensity, and to examine whether the frequency of flares was associated with back-related disability outcomes.</p> <p>Methods</p> <p>We conducted a cohort study of acute LBP patients utilizing frequent serial assessments and Internet-based data collection. Adults with acute LBP (lasting ≤3 months) completed questionnaires at the time of seeking care, and at both 3-day and 1-week intervals, for 6 weeks. Back pain was measured using a numerical pain rating scale (NPRS), and disability was measured using the Oswestry Disability Index (ODI). A pain flare was defined as 'a period of increased pain lasting at least 2 hours, when your pain intensity is distinctly worse than it has been recently'. We used mixed-effects linear regression to model longitudinal changes in pain intensity, and multivariate linear regression to model associations between flare frequency and disability outcomes.</p> <p>Results</p> <p>42 of 47 participants (89%) reported pain flares, and the average number of discrete flare periods per patient was 3.5 over 6 weeks of follow-up. More than half of flares were less than 4 hours in duration, and about 75% of flares were less than one day in duration. A model with a quadratic trend for time best characterized improvements in pain. Pain decreased rapidly during the first 14 days after seeking care, and leveled off after about 28 days. Patients who reported a pain flare experienced an almost 3-point greater current NPRS than those not reporting a flare (mean difference [SD] 2.70 [0.11]; p < 0.0001). Higher flare frequency was independently associated with a higher final ODI score (<it>ß </it>[SE} 0.28 (0.08); p = 0.002).</p> <p>Conclusions</p> <p>Acute LBP is characterized by variability. Patients with acute LBP report multiple distinct flares of pain, which correspond to discrete increases in pain intensity. A higher flare frequency is associated with worse disability outcomes.</p

The Grizzly, September 5, 2013

New Policy Changes • Social Host to Event Director • Printing with Bear Bucks • Grizzly Launches Web Redesign • Farmers Market Location Changes • Community Service • Travel Blog Preview • Ursinus Alumni Return for Work • Opinion: Smart Phone Addiction Can Harm Our Social Lives; North and New Need Single Sex Hall Options Too • Code of Conduct for Athletes Now an Official Contract • Football Preview: Experienced Bears Major Asset • Field Hockey Looks to Regain Conference Dominancehttps://digitalcommons.ursinus.edu/grizzlynews/1884/thumbnail.jp