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INTRODUCTION/AIMS: Intercostal nerve injury can occur after rib fractures, resulting in denervation of the abdominal musculature. Loss of innervation to the rectus abdominis and intercostal muscles can cause pain, atrophy, and eventual eventration, which may be an underrecognized and thus undertreated complication of rib fractures. We investigated the clinical utility of intercostal nerve electrodiagnostic testing following rib fractures to diagnose and localize nerve injury at levels T7 and below. METHODS: Five patients with displaced bicortical rib fractures involving the 7th-11th ribs and clinical eventration of the ipsilateral abdominal wall underwent intercostal nerve conduction studies (NCS) and needle electromyography (EMG) on the affected side. EMG of the rectus abdominis and intercostal muscles was performed with ultrasound guidance, and ultrasound measurements of rectus abdominis thickness were obtained to assess for atrophy. RESULTS: Average patient age was 59.4 years and average body mass index (BMI) was 31.5 kg/m2. Intercostal NCS and EMG were able to reliably diagnose and localize intercostal nerve damage after rib fractures. Ultrasound demonstrated an average rectus abdominis transverse cross-sectional thickness of 0.534 cm on the affected side, compared with 1.024 cm on the non-affected side. DISCUSSION: Intercostal electrodiagnostic studies can diagnose and localize intercostal nerve damage after displaced rib fractures. Musculoskeletal ultrasound can be used to diagnose and quantify rectus abdominis atrophy and to accurately and safely guide needle EMG to the intercostal and rectus abdominis muscles.
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Malaria is caused when Plasmodium sporozoites are injected along with saliva by an anopheline mosquito into the dermis of a vertebrate host. Arthropod saliva has pleiotropic effects that can influence local host responses, pathogen transmission, and exacerbation of the disease. A mass spectrometry screen identified mosquito salivary proteins that are associated with Plasmodium sporozoites during saliva secretions. In this study, we demonstrate that one of these salivary antigens, Anopheles gambiae sporozoite-associated protein (AgSAP), interacts directly with Plasmodium falciparum and Plasmodium berghei sporozoites. AgSAP binds to heparan sulfate and inhibits local inflammatory responses in the skin. The silencing of AgSAP in mosquitoes reduces their ability to effectively transmit sporozoites to mice. Moreover, immunization with AgSAP decreases the Plasmodium burden in mice that are bitten by Plasmodium-infected mosquitoes. These data suggest that AgSAP facilitates early Plasmodium infection in the vertebrate host and serves as a target for the prevention of malaria. IMPORTANCE Malaria is a vector-borne disease caused by Plasmodium sporozoites. When an anopheline mosquito bites its host, it releases Plasmodium sporozoites as well as saliva components. Mosquito proteins have the potential to serve as antigens to prevent or influence malaria without directly targeting the pathogen. This may help set a new paradigm for vaccine development. In this study, we have elucidated the role of a novel salivary antigen, named Anopheles gambiae sporozoite-associated protein (AgSAP). The results presented here show that AgSAP interacts with Plasmodium falciparum and Plasmodium berghei sporozoites and modulates local inflammatory responses in the skin. Furthermore, our results show that AgSAP is a novel mosquito salivary antigen that influences the early stages of Plasmodium infection in the vertebrate host. Individuals living in countries where malaria is endemic generate antibodies against AgSAP, which indicates that AgSAP can serve as a biomarker for disease prevalence and epidemiological analysis.