Impact of the COVID-19 pandemic on emergency department CT for suspected diverticulitis.

PURPOSE: This study examined the impact of the COVID-19 pandemic on emergency department CT use for acute nontraumatic abdominal pain, to better understand why imaging volume so drastically decreased during the COVID-19 pandemic. METHODS: This was a retrospective review of emergency imaging volumes from January 5 to May 30, 2020. Weekly volume data were collected for total imaging studies, abdominopelvic CT, and abdominopelvic CTs positive for common causes of acute nontraumatic abdominal pain. Two emergency radiology attendings scored all diverticulitis cases independently, and weekly volume data for uncomplicated and complicated diverticulitis cases was also collected. Volume data prior to and during the COVID-19 pandemic was compared, using 2019 volumes as a control. RESULTS: During the COVID-19 pandemic, overall emergency imaging volume decreased 30% compared to 2019 (p = 0.002). While the number of emergency abdominopelvic CTs positive for appendicitis and small bowel obstruction did not significantly change during the COVID-19 pandemic, the number of cases of diverticulitis decreased significantly compared to 2019 (p = 0.001). This reduction can be specifically attributed to decreased uncomplicated diverticulitis cases, as the number of uncomplicated diverticulitis cases dropped significantly (p = 0.002) while there was no significant difference in the number of complicated diverticulitis cases (p = 0.09). CONCLUSIONS: Reduced emergency abdominopelvic CT volume during the COVID-19 pandemic can partially be explained by decreased imaging of lower acuity patients. This data may help formulate future strategies for imaging resource utilization with an improved understanding of the relationship between perceived imaging risk and symptom acuity.

Bioluminescence and second harmonic generation imaging reveal dynamic changes in the inflammatory and collagen landscape in early osteoarthritis.

Osteoarthritis (OA) is a leading cause of chronic disability whose mechanism of pathogenesis is largely elusive. Local inflammation is thought to play a key role in OA progression, especially in injury-associated OA. While multiple inflammatory cytokines are detected, the timing and extent of overall inflammatory activities in early OA and the manner by which joint inflammation correlates with cartilage structural damage are still unclear. We induced OA via destabilization of the medial meniscus (DMM) in NFκB luciferase reporter mice, whose bioluminescent signal reflects the activity of NFκB, a central mediator of inflammation. Bioluminescence imaging data showed that DMM and sham control joints had a similar surge of inflammation at 1-week post-surgery, but the DMM joint exhibited a delay in resolution of inflammation in subsequent weeks. A similar trend was observed with synovitis, which we found to be mainly driven by synovial cell density and inflammatory infiltration rather than synovial lining thickness. Interestingly, an association between synovitis and collagen structural damage was observed in early OA. Using Second Harmonic Generation (SHG) imaging, we analyzed collagen fiber organization in articular cartilage. Zonal differences in collagen fiber thickness and organization were observed as soon as OA initiated after DMM surgery, and persisted over time. Even at 1-week post-surgery, the DMM joint showed a decrease in collagen fiber thickness in the deep zone and an increase in collagen fiber disorganization in the superficial zone. Since we were able detect and quantify collagen structural changes very early in OA development by SHG imaging, we concluded that SHG imaging is a highly sensitive tool to evaluate pathological changes in OA. In summary, this study uncovered a dynamic profile of inflammation and joint cartilage damage during OA initiation and development, providing novel insights into OA pathology.

Shedding Light on T2 Bright Masses on Breast MRI: Benign and Malignant Causes.

While T2 hyperintense masses on breast MRI are often benign, there are several malignant etiologies that can also be T2 hyperintense. Delineation between benign and malignant entities is important for the accurate interpretation of breast MRI. Common benign T2 hyperintense masses include cysts, fibroadenomas, and lymph nodes. Malignant processes that are T2 hyperintense include metastatic lymph nodes, mucinous breast carcinomas, papillary breast carcinomas, and breast cancers with central necrosis. Evaluation of the morphology and enhancement pattern of a T2 hyperintense mass can help to differentiate a benign process from a malignant one. This educational review will present both benign and malignant causes of T2 hyperintense masses on breast MRI and review common imaging findings and pertinent imaging characteristics that can be used to help accurately identify benign entities while also recognizing suspicious lesions that require additional evaluation.

Wnt7a Inhibits IL-1ß Induced Catabolic Gene Expression and Prevents Articular Cartilage Damage in Experimental Osteoarthritis.

Wnt7a is a protein that plays a critical role in skeletal development. However, its effect on cartilage homeostasis under pathological conditions is not known. In this study, we found a unique inverse correlation between Wnt7a gene expression and that of MMP and IL-1ß in individual human OA cartilage specimens. Upon ectopic expression in primary human articular chondrocytes, Wnt7a inhibited IL-1ß-induced MMP and iNOS gene expression. Western blot analysis indicated that Wnt7a induced both canonical Wnt signaling and NFAT and Akt non-canonical signaling. Interestingly, inhibiting the canonical and Akt pathway did not affect Wnt7a activity. However, inhibiting the NFAT pathway impaired Wnt7a's ability to inhibit MMP expression, suggesting that Wnt7a requires NFAT signaling to exert this function. In vivo, intraarticular injection of lentiviral Wnt7a strongly attenuated articular cartilage damage induced by destabilization of the medial meniscus (DMM) OA-inducing surgery in mice. Consistently, Wnt7a also inhibited the progressive increase of joint MMP activity in DMM animals. These results indicate that Wnt7a signaling inhibits inflammatory stimuli-induced catabolic gene expression in human articular chondrocytes and is sufficient to attenuate MMP activities and promote joint cartilage integrity in mouse experimental OA, demonstrating a novel effect of Wnt7a on regulating OA pathogenesis.