BACKGROUND: Abnormal scaphoid alignment after fracture is used as an indication for fixation. Acceptable alignment after reduction and fixation of scaphoid fractures is not well defined. We systematically reviewed the literature to identify how scaphoid malunion is currently defined and by what parameters. METHODS: A systematic review was performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Multiple databases were searched for studies published in the English language that reported on outcomes after scaphoid malunion and included measurements to define malunions. Radiographic scaphoid measurement parameters were collected. Clinical outcome measures recorded included grip strength, wrist range of motion, and patient-reported outcome measures. Study quality was analyzed using the Methodological Index for Non-Randomized Studies (MINORS) criteria. Descriptive summaries of the studies are presented. RESULTS: The initial search yielded 1600 articles. Ten articles (161 participants, 93% males, mean age = 28.3 + 6.3 years, mean MINORS score = 10.2 + 1.6) were included and analyzed. Scaphoid malunion was defined if the lateral intrascaphoid angle (LISA) was >45° (3 articles), LISA >35° (1 article), and height to length ratio >0.6 (3 articles). Four out of 5 studies found no significant associations between patient outcomes and degree of scaphoid malunion measured on imaging. CONCLUSIONS: There is a lack of consensus for defining scaphoid malunion on imaging and absence of correlation between findings on imaging and patient outcomes. Future studies defining scaphoid malunion should be appropriately powered, incorporate measures of intrarater and interrater reliabilities for all reported imaging measurements, and utilize validated patient-reported outcome measures to reflect that malunion is associated with inferior outcomes meaningful to patients.

Background and aims

Use of GI endoscopy is historically lower in nonwhite ethnic and racial groups compared with whites. These disparities are multifactorial but likely contribute to differences in GI clinical outcomes. We sought to improve endoscopy uptake overall and in minorities by predictive overbooking and active recruitment in a hospital-based GI clinic.

Methods

From January to October 2014, we alternated between traditional booking for Veterans Affairs Healthcare Network patients with a physician recommendation for endoscopy and active recruitment of patients to fill projected open endoscopy appointment slots. On intervention weeks, patients attending a GI clinic were given the opportunity to "fast track" to an endoscopy appointment on short notice. During control weeks, patients were not actively recruited. We compared uptake of endoscopy appointments in both groups and performed logistic regression to determine predictors of participation in fast-track active recruitment.

Results

During fast-track active recruitment for endoscopy, the clinic recruited an additional 111 patients for endoscopy over passive recruitment, including 46 African Americans (41.4%). In a logistic regression model controlling for demographic and clinical characteristics, African Americans were twice as likely (adjusted OR, 1.99; 95% CI, 1.26-3.17) than whites to participate in the fast-track option for recommended endoscopy.

Conclusions

Interventions to actively recruit patients for endoscopy increased the overall percentage of GI clinic patients undergoing endoscopy and disproportionately improved endoscopy appointment uptake in African Americans.

Structure-mechanism relationships are key determinants of host defense peptide efficacy. These relationships are influenced by anatomic, physiologic and microbiologic contexts. Structure-mechanism correlates were assessed for the synthetic peptide RP-1, modeled on microbicidal domains of platelet kinocidins. Antimicrobial efficacies and mechanisms of action against susceptible (^S) or resistant (^R) Salmonella typhimurium (ST), Staphylococcus aureus (SA), and Candida albicans (CA) strain pairs were studied at pH 7.5 and 5.5. Although RP-1 was active against all study organisms, it exhibited greater efficacy against bacteria at pH 7.5, but greater efficacy against CA at pH 5.5. RP-1 de-energized SA and CA, but caused hyperpolarization of ST in both pH conditions. However, RP-1 permeabilized ST^S and CA strains at both pH, whereas permeabilization was modest for ST^R or SA strain at either pH. Biochemical analysis, molecular modeling, and FTIR spectroscopy data revealed that RP-1 has indistinguishable net charge and backbone trajectories at pH 5.5 and 7.5. Yet, concordant with organism-specific efficacy, surface plasmon resonance, and FTIR, molecular dynamics revealed modest helical order increases but greater RP-1 avidity and penetration of bacterial than eukaryotic lipid systems, particularly at pH 7.5. The present findings suggest that pH– and target–cell lipid contexts influence selective antimicrobial efficacy and mechanisms of RP-1 action. These findings offer new insights into selective antimicrobial efficacy and context–specificity of antimicrobial peptides in host defense, and support design strategies for potent anti-infective peptides with minimal concomitant cytotoxicity.

Prions consist of pathological aggregates of cellular prion protein and have the ability to replicate, causing neurodegenerative diseases, a phenomenon mirrored in many other diseases connected to protein aggregation, including Alzheimer's and Parkinson's diseases. However, despite their key importance in disease, the individual processes governing this formation of pathogenic aggregates, as well as their rates, have remained challenging to elucidate in vivo. Here we bring together a mathematical framework with kinetics of the accumulation of prions in mice and microfluidic measurements of aggregate size to dissect the overall aggregation reaction into its constituent processes and quantify the reaction rates in mice. Taken together, the data show that multiplication of prions in vivo is slower than in in vitro experiments, but efficient when compared with other amyloid systems, and displays scaling behavior characteristic of aggregate fragmentation. These results provide a framework for the determination of the mechanisms of disease-associated aggregation processes within living organisms.