Return to Sport After Turf Toe Injuries: A Systematic Review and Meta-analysis

A grant from the One-University Open Access Fund at the University of Kansas was used to defray the author's publication fees in this Open Access journal. The Open Access Fund, administered by librarians from the KU, KU Law, and KUMC libraries, is made possible by contributions from the offices of KU Provost, KU Vice Chancellor for Research & Graduate Studies, and KUMC Vice Chancellor for Research. For more information about the Open Access Fund, please see http://library.kumc.edu/authors-fund.xml.Background: The prevalence of turf toe injuries has increased in recent years. However, uncertainty remains as to how to optimally treat turf toe injuries and the implications that the severity of the injury has on outcomes, specifically return to sport (RTS). Purpose: To determine RTS based on treatment modality and to provide clinicians with additional information when comparing operative versus nonoperative treatment of turf toe injuries in athletes. Study Design: Systematic review; Level of evidence, 4. Methods: A systematic review and meta-analysis was performed using the PubMed/Ovid MEDLINE/PubMed Central databases (May 1964 to August 2018) per PRISMA-IPD (Preferred Reporting Items for Systematic Reviews and Meta-Analyses of Individual Participant Data) guidelines. RTS, treatment, severity of injury, athletic position, and sport were recorded and analyzed. Results: Of 858 identified studies, 12 met the criteria for the final meta-analysis. The studies included 112 athletes sustaining a total of 121 turf toe injuries; 63 (52.1%) of these injuries were treated surgically, while 58 (47.9%) were treated nonoperatively, and 53.7% were classified by the grade of injury (grade I, n = 1; grade II, n = 9; grade III, n = 55). Overall, 56 (46.3%) injuries could not be classified based on the data provided and were excluded from the final analysis. The median time to RTS for patients treated nonoperatively was 5.85 weeks (range, 3.00-8.70 weeks) compared with 14.70 weeks (range, 6.00-156.43 weeks) for patients treated surgically (P < .001); however, there was variability in the grade of injury between the 2 groups. Similarly, patients who sustained grade II injuries returned to sport more quickly (8.70 weeks) than patients who had a grade I (13.04 weeks) or grade III injury (16.50 weeks) (P = .016). The amount of time required to RTS was significantly influenced by the athlete’s level of play (16.50 weeks for both high school and college levels; 14.70 weeks for professional level) (P = .018). Conclusion: The time to RTS for an athlete who suffers from a turf toe injury is significantly influenced by the severity of injury and the athlete’s level of competition. Professional athletes who suffer from turf toe injuries RTS sooner than both high school and college athletes. However, there are a limited number of high-level studies evaluating turf toe injuries in the athletic population. Further research is necessary to clearly define the appropriate treatment and RTS protocols based on sport, position, and level of play

The KGD Motif of Epstein-Barr Virus gH/gL Is Bifunctional, Orchestrating Infection of B Cells and Epithelial Cells

Epstein-Barr virus (EBV), a member of the herpesvirus family, is the causative agent of common human infections and specific malignancies. EBV entry into target cells, including B cells and epithelial cells, requires the interaction of multiple virus-encoded glycoproteins. Glycoproteins H and L (gH/gL) cooperate with glycoprotein B (gB) to mediate fusion of the viral envelope with target cell membranes. Both the gH/gL complex and gB are required for fusion, whereas glycoprotein 42 (gp42) acts as a tropism switch and is required for B cell infection and inhibits epithelial cell infection. Our previous studies identified a prominent KGD motif located on the surface of gH/gL. In the current study, we found that this motif serves as a bifunctional domain on the surface of gH/gL that directs EBV fusion of B cells and epithelial cells. Mutation of the KGD motif to AAA decreased fusion with both epithelial and B cells and reduced the binding of gH/gL to epithelial cells and to gp42. We also demonstrate that deletion of amino acids 62 to 66 of gp42 selectively reduces binding to wild-type gH/gL, but not the KGD mutant, suggesting that the KGD motif of gH/gL interacts with the N-terminal amino acids 62 to 66 of gp42

A randomized placebo-controlled study on the effect of nifedipine on coronary endothelial function and plaque formation in patients with coronary artery disease: the ENCORE II study†

Aims Endothelial dysfunction and plaque formation are features of atherosclerosis. Inhibition of L-type calcium channels or HMG-CoA pathway improves endothelial function and reduces plaque size. Thus, we investigated in stable coronary artery disease (CAD) the effects of a calcium antagonist on coronary endothelial function and plaque size. Methods and results In 454 patients undergoing PCI, acetylcholine (10−6 to 10−4 M) was infused in a coronary segment without significant CAD. Changes in coronary diameter were measured and an intravascular ultrasound examination (IVUS) was performed. On top of statin therapy, patients were randomized in a double-blind fashion to placebo or nifedipine GITS 30-60 mg/day and followed for 18-24 months. Blood pressure was lower on nifedipine than on placebo by 5.8/2.1 mmHg (P < 0.001) as was total and LDL cholesterol (4.8 mg/dL; P = 0.495), while HDL was higher (3.6 mg/dL; P = 0.026). In the most constricting segment, nifedipine reduced vasoconstriction to acetylcholine (14.0% vs. placebo 7.7%; P < 0.0088). The percentage change in plaque volume with nifedipine and placebo, respectively, was 1.0 and 1.9%, ns. Conclusion The ENCORE II trial demonstrates in a multi-centre setting that calcium channel blockade with nifedipine for up to 2 years improves coronary endothelial function on top of statin treatment, but did not show an effect of nifedipine on plaque volum

Forty years of carabid beetle research in Europe - from taxonomy, biology, ecology and population studies to bioindication, habitat assessment and conservation

Volume: 100Start Page: 55End Page: 14

Ablation of mouse adult neurogenesis alters olfactory bulb structure and olfactory fear conditioning

Adult neurogenesis replenishes olfactory bulb (OB) interneurons throughout the life of most mammals, yet during this constant fl ux it remains unclear how the OB maintains a constant structure and function. In the mouse OB, we investigated the dynamics of turnover and its impact on olfactory function by ablating adult neurogenesis with an x-ray lesion to the subventricular zone (SVZ). Regardless of the magnitude of the lesion to the SVZ, we found no change in the survival of young adult born granule cells (GCs) born after the lesion, and a gradual decrease in the population of GCs born before the lesion. After a lesion producing a 96% reduction of incoming adult born GCs to the OB, we found a diminished behavioral fear response to conditioned odor cues but not to audio cues. Interestingly, despite this behavioral defi cit and gradual anatomical changes, we found no electrophysiological changes in the GC population assayed in vivo through dendro-dendritic synaptic plasticity and odor-evoked local fi eld potential oscillations. These data indicate that turnover in the granule cell layer is generally decoupled from the rate of adult neurogenesis, and that OB adult neurogenesis plays a role in a wide behavioral system extending beyond the OB