Daily Reports on Phage-Host Interactions.

Understanding phage-host relationships is crucial for the study of virus biology and the application of phages in biotechnology and medicine. However, information concerning the range of hosts for bacterial and archaeal viruses is scattered across numerous databases and is difficult to obtain. Therefore, here we present PHD (Phage & Host Daily), a web application that offers a comprehensive, up-to-date catalog of known phage-host associations that allows users to select viruses targeting specific bacterial and archaeal taxa of interest. Our service combines the latest information on virus-host interactions from seven source databases with current taxonomic classification retrieved directly from the groups and institutions responsible for its maintenance. The web application also provides summary statistics on host and virus diversity, their pairwise interactions, and the host range of deposited phages. PHD is updated daily and available at http://phdaily.info or http://combio.pl/phdaily.

The Turtle Neck Sign: Identification of Severe Retracted Distal Biceps Tendon Rupture.

BACKGROUND: Chronic tendon retraction subsequent to distal biceps tendon rupture significantly increases repair difficulty and potential for tendon grafting. Biceps tendons that appear short or absent with magnetic resonance imaging (MRI) or that cannot be readily identified at surgery may erroneously be classified as irreparable. These apparent "absent" biceps tendons may actually be retracted and curled up inside the muscle, visually resembling the head-neck of a turtle retracted inside its shell (the "turtle neck sign"). When located, these tendons could be unfolded and repaired primarily. This type of tendon retraction seems to be associated with high-degree ruptures and larcertus fibrosus tears. PURPOSE: To test the hypothesis that tendon retractions with a turtle neck sign on MRI are more associated with high-degree ruptures and larcertus fibrosus tears versus tendon tears with simple linear retraction. STUDY DESIGN: Cross-sectional study; Level of evidence, 3. METHODS: Retracted distal biceps tendon ruptures on sagittal MRI were categorized as linear retraction or curled-up (turtle neck) retraction. Retraction length, injury severity, and lacertus fibrosus tears were analyzed. RESULTS: The authors retrospectively analyzed the patient records of 85 consecutive traumatic distal biceps tendon ruptures from 2003 to 2019; the final study cohort was 37 patients. Injury-to-surgery timing was as follows: <3 weeks, 43% (16 cases); 3 weeks to 3 months, 32% (12 cases); and >3 months, 24% (9 cases). Overall, 19 patients had linear retraction <7 cm (mean, 3.3 ± 1.9 cm) and 18 patients had a turtle neck retraction ≥7 cm (mean, 9.1 ± 1.6 cm). The injury-to-surgery time (median [± interquartile range]) was 27 days (±90 days) in the linear retraction group and 23 days (±65 days) in the turtle neck retraction group. The turtle neck retraction group had a significantly higher occurrence of abnormal hook test findings, complete distal biceps tendon rupture, and lacertus fibrosus tears compared with the linear retraction group (100% vs 58%, 100% vs 68%, and 100% vs 37%, respectively; P ≤ .02). However, significant repairability differences were not found. CONCLUSION: Highly retracted distal biceps turtle neck sign tendon ruptures occur frequently in association with high-degree ruptures and lacertus fibrosus tears. The presence of a turtle neck retraction did not affect reparability. Surgeons should be aware of this curled-up retraction to avoid mistaking it for an absent tendon or a muscle-tendon disruption.

Human dystrophin expressing chimeric (DEC) cell therapy ameliorates cardiac, respiratory, and skeletal muscle's function in Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a progressive and lethal disease, caused by X-linked mutations of the dystrophin encoding gene. The lack of dystrophin leads to muscle weakness, degeneration, fibrosis, and progressive loss of skeletal, cardiac, and respiratory muscle function resulting in premature death due to the cardiac and respiratory failure. There is no cure for DMD and current therapies neither cure nor arrest disease progression. Thus, there is an urgent need to develop new approaches and safer therapies for DMD patients. We have previously reported functional improvements which correlated with increased dystrophin expression following transplantation of dystrophin expressing chimeric (DEC) cells of myoblast origin to the mdx mouse models of DMD. In this study, we demonstrated that systemic-intraosseous transplantation of DEC human cells derived from myoblasts of normal and DMD-affected donors, increased dystrophin expression in cardiac, respiratory, and skeletal muscles of the mdx/scid mouse model of DMD. DEC transplant correlated with preservation of ejection fraction and fractional shortening on echocardiography, improved respiratory function on plethysmography, and improved strength and function of the limb skeletal muscles. Enhanced function was associated with improved muscle histopathology, revealing reduced mdx pathology, fibrosis, decreased inflammation, and preserved muscle morphology and architecture. Our findings confirm that DECs generate a systemic protective effect in DMD-affected target organs. Therefore, DECs represents a novel therapeutic approach with the potential to preserve or enhance multiorgan function of the skeletal, cardiac, and respiratory muscles critical for the well-being of DMD patients.