Location and Size of the Reverse Hill-Sachs Lesion in Patients with Traumatic Posterior Shoulder Instability.

BACKGROUND: In patients with traumatic posterior shoulder instability, little is known about the precise location and size of the reverse Hill-Sachs lesion. METHODS: Forty-nine shoulders of 47 patients with traumatic posterior instability were included in this study based on the following inclusion criteria: 1) a primary or recurrent traumatic posterior shoulder dislocation, and 2) the initial event was caused by trauma. Patients were excluded if they had: 1) no history of trauma, 2) prior shoulder surgery, 3) no CT examination, or 4) seizure cases. Three-dimensional images of the humerus reconstructed from CT images were reviewed using an image analysis software. The location and size of the reverse Hill-Sachs lesion were measured and described on a clock face on the humeral head. RESULTS: The reverse Hill-Sachs lesion was observed in 25 of 49 shoulders (51%). The reverse Hill-Sachs lesions were located between 1:37 and 2:48. The depth of the reverse Hill-Sachs lesion (mean ± SD) was 5.8 ± 2.2 mm. The extent of the reverse Hill-Sachs lesion was 35° ± 12°. The average orientation of the reverse Hill-Sachs lesion, represented by an angle measured from the 12 o'clock position, was 64° ± 12° and pointing towards 2:09 on a clock face. Length and width of reverse Hill-Sachs lesions were 9.7 ± 4.7 mm, 11.1 ± 3.6 mm, respectively. CONCLUSION: The reverse Hill-Sachs lesion was a semicircular compression fracture located on the anteromedial aspect of the humeral head. Compared with shoulders with anterior shoulder instability, the humeral defect was smaller and located more inferiorly in shoulders with posterior instability.

Effects of predator modulation and vector preference on pathogen transmission in plant populations.

Biological control programs frequently rely on predators to control vector-borne pathogens by consumptive effects on vector abundance in agroecosystems. Meanwhile, the spread of vectored disease depends on the vector preference for host status (healthy or infected hosts). Yet, it is unclear how vector preferences alter the controlled effectivity of predators in pathogen transmission. Therefore, we here addressed the plant-vector-pathogen models assessing how pathogen transmission in plant was affected by variable predation rates and vector preferences for host status. Specifically, we discussed effects of predators on vector abundance and pathogen transmission under both a non-spatial model and a spatially structured metapopulation model. We showed that predators can decrease the vector abundance and inhibit pathogen prevalence, whereas vector preference contributes profoundly to the controlled effectivity of predators on the spread of vector-borne pathogens. Moreover, predation can increase oscillation amplitude of the pathogen prevalence in both plant and vector; suggesting that the inclusion of predator can amplify the effects of environmental stochasticity on pathogen dynamics. In conclusion, our results support the prediction of theoretical disease models showing predator can be a natural enemy for pathogen control, and also extend that predatory interactions interacting with vector preferences play the singularly joint effects on the spread of vector-borne pathogens.