Novice Interpreters, American Sign Language Proficiency, and the National Interpreter Certification Performance Exam

More than 40 years after American Sign Language (ASL) and interpreter education were first offered as programs of study in higher education, little is known about the level of ASL proficiency of graduates from baccalaureate degree programs in interpreting and what level of ASL proficiency may be associated with passing the performance portion of the National Interpreter Certification (NIC) examination. With this in mind, we posed three questions: 1) What is the distribution of ASL Proficiency Interview (ASLPI) ratings of a national sample of novice interpreters relatively near the time of graduation from baccalaureate degree programs in interpreting? 2) What is the distribution of ASLPI ratings of a national sample of novice interpreters relatively near the time of taking the NIC Performance Exam? 3) What is the relationship between ASLPI ratings and passing/not passing the NIC Performance Exam? Results showed that relatively closer to IEP graduation (N = 134), about 56% of ASLPI proficiency levels were at or below Level 2+ and 44% were at or above Level 3. For ASLPI proficiency levels obtained relatively closer to taking the NIC Performance Exam (N = 154), about 30% were at or below Level 2+ and 70% of ratings were at or above Level 3. Results showed that all those who passed the NIC Performance Exam, and who had a rating for the ASLPI taken relatively closer to taking the NIC Performance Exam (N = 27), obtained an ASLPI proficiency level of 3 or higher. However, it is important to note that approximately 75% of participants who obtained a proficiency level of 3 or higher did not pass the NIC Performance Exam the first time they took it. Additionally, the higher the ASLPI level, the higher the proportion of people passing the NIC Performance Exam. This study has implications for further research regarding ASL proficiency for students entering and exiting IEPs and preparing for national credentialing

Comprehensive molecular pharmacology screening reveals potential new receptor interactions for clinically relevant opioids

Most clinically used opioids are thought to induce analgesia through activation of the mu opioid receptor (MOR). However, disparities have been observed between the efficacy of opioids in activating the MOR in vitro and in inducing analgesia in vivo. In addition, some clinically used opioids do not produce cross-tolerance with each other, and desensitization produced in vitro does not match tolerance produced in vivo. These disparities suggest that some opioids could be acting through other targets in vivo, but this has not been comprehensively tested. We thus screened 9 clinically relevant opioids (buprenorphine, hydrocodone, hydromorphone, morphine, 0-desmethyl-tramadol, oxycodone, oxymorphone, tapentadol, tramadol) against 9 pain-related receptor targets (MOR, delta opioid receptor [DOR], kappa opioid receptor [KOR], nociceptin receptor [NOP], cannabinoid receptor type 1 [CB1], sigma-1 receptor [al R], and the monoamine transporters [NET/SERT/DAT]) expressed in cells using radioligand binding and functional activity assays. We found several novel interactions, including monoamine transporter activation by buprenorphine and al R binding by hydrocodone and tapentadol. Tail flick anti-nociception experiments with CD-1 mice demonstrated that the monoamine transporter inhibitor duloxetine selectively promoted buprenorphine anti-nociception while producing no effects by itself or in combination with the most MOR-selective drug oxymorphone, providing evidence that these novel interactions could be relevant in vivo. Our findings provide a comprehensive picture of the receptor interaction profiles of clinically relevant opioids, which has not previously been performed. Our findings also suggest novel receptor interactions for future investigation that could explain some of the disparities observed between opioid performance in vitro and in vivo.Depomed, Inc.; University of ArizonaOpen 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]

Urine proteomics in the diagnosis of stable angina.

BACKGROUND: We have previously described a panel of 238 urinary polypeptides specific for established severe coronary artery disease (CAD). Here we studied this polypeptide panel in patients with a wider range of CAD severity. METHODS: We recruited 60 patients who underwent elective coronary angiography for investigation of stable angina. Patients were selected for either having angiographic evidence of CAD or not (NCA) following coronary angiography (n = 30/30; age, 55 ± 6 vs. 56 ± 7 years, P = 0.539) to cover the extremes of the CAD spectrum. A further 66 patients with severe CAD (age, 64 ± 9 years) prior to surgical coronary revascularization were added for correlation studies. The Gensini score was calculated from coronary angiograms as a measure of CAD severity. Urinary proteomic analyses were performed using capillary electrophoresis coupled online to micro time-of-flight mass spectrometry. The urinary polypeptide pattern was classified using a predefined algorithm and resulting in the CAD238 score, which expresses the pattern quantitatively. RESULTS: In the whole cohort of patients with CAD (Gensini score 60 [40; 98]) we found a close correlation between Gensini scores and CAD238 (ρ = 0.465, P < 0.001). After adjustment for age (β = 0.144; P = 0.135) the CAD238 score remained a significant predictor of the Gensini score (β =0.418; P < 0.001). In those with less severe CAD (Gensini score 40 [25; 61]), however, we could not detect a difference in CAD238 compared to patients with NCA (-0.487 ± 0.341 vs. -0.612 ± 0.269, P = 0.119). CONCLUSIONS: In conclusion the urinary polypeptide CAD238 score is associated with CAD burden and has potential as a new cardiovascular biomarker

Duration of Rheumatoid Arthritis and the Risk of Developing Interstitial Lung Disease

Age of ILD onset is similar in patients with RA-UIP and RA-NSIP but duration of RA before ILD onset differs

Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.

GWAS have identified a breast cancer susceptibility locus on 2q35. Here we report the fine mapping of this locus using data from 101,943 subjects from 50 case-control studies. We genotype 276 SNPs using the 'iCOGS' genotyping array and impute genotypes for a further 1,284 using 1000 Genomes Project data. All but two, strongly correlated SNPs (rs4442975 G/T and rs6721996 G/A) are excluded as candidate causal variants at odds against &gt;100:1. The best functional candidate, rs4442975, is associated with oestrogen receptor positive (ER+) disease with an odds ratio (OR) in Europeans of 0.85 (95% confidence interval=0.84-0.87; P=1.7 × 10(-43)) per t-allele. This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin