The posterior crescent sign on MRI and MR arthrography: is it a marker of hip dysplasia and instability?

OBJECTIVE: To evaluate the prevalence of the 'posterior crescent sign' in symptomatic patients referred for MRI/MR arthrogram of the hip and identify any correlation with imaging features of joint pathology. MATERIALS AND METHODS: Retrospective imaging assessment of a cohort of 1462 hips, from 1380 included MR examinations (82 bilateral) retrieved from a search of all examinations in patients 16-50 years old from June 2018 to June 2021, with median age 45.8 years (range 17.8-50.0) and 936 hips (64%) in women. Radiographic and MR findings related to hip dysplasia, femoroacetabular impingement and osteoarthritis were assessed. RESULTS: Fifty-one hips (3.5%) were positive for the posterior crescent sign, median age of 45.8 years (range 17.8-50.0) and 29 (58%) in women. Radiographic findings included the following: mean lateral centre edge angle (LCEA) 22.2° (± 7.8°) with LCEA < 20° in 15 (31%) and LCEA 20-25° in 17 (35%) and mean acetabular index (AI) of 13.1° (± 5.8°) with AI > 13° in 22 (45%). MR findings included the following: mean anterior acetabular sector angle (AASA) 54.3° (± 9.8°), mean posterior acetabular sector angle (PASA) 92.7° (± 7.0°), labral tear at 3-4 o'clock in 20 (39%), high-grade acetabular chondral loss in 42 (83%) and ligamentum teres abnormality in 20 (39%). CONCLUSION: The posterior crescent sign occurs in 3.5% of symptomatic young and middle-aged adults on MR. It is associated with overt and borderline hip dysplasia and other findings of hip instability. It is also associated with osteoarthritis in some cases and should be interpreted with caution in these patients.

RELMα Licenses Macrophages for Damage-Associated Molecular Pattern Activation to Instigate Pulmonary Vascular Remodeling.

Pulmonary hypertension (PH) is a debilitating disease characterized by remodeling of the lung vasculature. In rodents, resistin-like molecule-α (RELMα, also known as HIMF or FIZZ1) can induce PH, but the signaling mechanisms are still unclear. In this study, we used human lung samples and a hypoxia-induced mouse model of PH. We found that the human homolog of RELMα, human (h) resistin, is upregulated in macrophage-like inflammatory cells from lung tissues of patients with idiopathic PH. Additionally, at PH onset in the mouse model, we observed RELMα-dependent lung accumulation of macrophages that expressed high levels of the key damage-associated molecular pattern (DAMP) molecule high-mobility group box 1 (HMGB1) and its receptor for advanced glycation end products (RAGE). In vitro, RELMα/hresistin-induced macrophage-specific HMGB1/RAGE expression and facilitated HMGB1 nucleus-to-cytoplasm translocation and extracellular secretion. Mechanistically, hresistin promoted HMGB1 posttranslational lysine acetylation by preserving the NAD+-dependent deacetylase sirtuin (Sirt) 1 in human macrophages. Notably, the hresistin-stimulated macrophages promoted apoptosis-resistant proliferation of human pulmonary artery smooth muscle cells in an HMGB1/RAGE-dependent manner. In the mouse model, RELMα also suppressed the Sirt1 signal in pulmonary macrophages in the early posthypoxic period. Notably, recruited macrophages in the lungs of these mice carried the RELMα binding partner Bruton tyrosine kinase (BTK). hResistin also mediated the migration of human macrophages by activating BTK in vitro. Collectively, these data reveal a vascular-immune cellular interaction in the early PH stage and suggest that targeting RELMα/DAMP-driven macrophages may offer a promising strategy to treat PH and other related vascular inflammatory diseases.

HIMF (Hypoxia-Induced Mitogenic Factor) Signaling Mediates the HMGB1 (High Mobility Group Box 1)-Dependent Endothelial and Smooth Muscle Cell Crosstalk in Pulmonary Hypertension.

OBJECTIVE: HIMF (hypoxia-induced mitogenic factor; also known as FIZZ1 [found in inflammatory zone-1] or RELM [resistin-like molecule-α]) is an etiological factor of pulmonary hypertension (PH) in rodents, but its underlying mechanism is unclear. We investigated the immunomodulatory properties of HIMF signaling in PH pathogenesis. Approach and Results: Gene-modified mice that lacked HIMF (KO [knockout]) or overexpressed HIMF human homolog resistin (hResistin) were used for in vivo experiments. The pro-PH role of HIMF was verified in HIMF-KO mice exposed to chronic hypoxia or sugen/hypoxia. Mechanistically, HIMF/hResistin activation triggered the HMGB1 (high mobility group box 1) pathway and RAGE (receptor for advanced glycation end products) in pulmonary endothelial cells (ECs) of hypoxic mouse lungs in vivo and in human pulmonary microvascular ECs in vitro. Treatment with conditioned medium from hResistin-stimulated human pulmonary microvascular ECs induced an autophagic response, BMPR2 (bone morphogenetic protein receptor 2) defects, and subsequent apoptosis-resistant proliferation in human pulmonary artery (vascular) smooth muscle cells in an HMGB1-dependent manner. These effects were confirmed in ECs and smooth muscle cells isolated from pulmonary arteries of patients with idiopathic PH. HIMF/HMGB1/RAGE-mediated autophagy and BMPR2 impairment were also observed in pulmonary artery (vascular) smooth muscle cells of hypoxic mice, effects perhaps related to FoxO1 (forkhead box O1) dampening by HIMF. Experiments in EC-specific hResistin-overexpressing transgenic mice confirmed that EC-derived HMGB1 mediated the hResistin-driven pulmonary vascular remodeling and PH. CONCLUSIONS: In HIMF-induced PH, HMGB1-RAGE signaling is pivotal for mediating EC-smooth muscle cell crosstalk. The humanized mouse data further support clinical implications for the HIMF/HMGB1 signaling axis and indicate that hResistin and its downstream pathway may constitute targets for the development of novel anti-PH therapeutics in humans.

Bedside ultrasonography for acute gallstone disease: a diagnostic accuracy study of surgical registrars and emergency medicine physicians.

BACKGROUND: Acute gallstone disease, primarily biliary colic and acute cholecystitis, represents a significant burden on surgical services. Prolonged waiting times for ultrasonography to confirm a diagnosis contributes to inefficiency and delays surgery. Bedside ultrasound offers an opportunity for clinicians make a diagnosis more promptly and streamline acute surgery. This study evaluated the reliability of bedside ultrasound performed by clinicians following local training and a trial of its introduction into clinical practice. METHODS: This was a prospective inter-rater reliability study of bedside ultrasound scans performed on patients referred for suspected acute gallstone disease. Results were compared with a formal ultrasound scan in the radiology department. Inter-rater agreement for the finding of gallstones and the imaging diagnosis of acute cholecystitis was assessed. RESULTS: A total of 124 patients underwent bedside ultrasound scan, 87 (70.2%) performed by surgical registrars. Mean patient age was 48 years (range 19-92 years) with 95 females (76.6%). Inter-rater reliability for the finding of gallstones showed strong agreement with kappa 0.85 (95% confidence interval 0.76-0.95) whereas for the imaging diagnosis of acute cholecystitis there was a minimal agreement with kappa 0.37 (95% confidence interval 0.18-0.56). Sensitivity and specificity for the finding of gallstones on bedside ultrasound was 93% and 92%, respectively. CONCLUSION: Bedside ultrasound is accurate for the finding of gallstones, but the imaging diagnosis of acute cholecystitis is more challenging. There remains the potential for this to improve the efficiency of surgical assessment in suspected acute gallstone disease and this supports the ongoing provision of bedside ultrasound in surgical services.

Environmental control of the microfaunal community structure in tropical bromeliads.

Ecological communities hosted within phytotelmata (plant compartments filled with water) provide an excellent opportunity to test ecological theory and to advance our understanding of how local and global environmental changes affect ecosystems. However, insights from bromeliad phytotelmata communities are currently limited by scarce accounts of microfauna assemblages, even though these assemblages are critical in transferring, recycling, and releasing nutrients in these model ecosystems. Here, we analyzed natural microfaunal communities in leaf compartments of 43 bromeliads to identify the key environmental filters underlying their community structures. We found that microfaunal community richness and abundance were negatively related to canopy openness and vertical height above the ground. These associations were primarily driven by the composition of amoebae and flagellate assemblages and indicate the importance of bottom-up control of microfauna in bromeliads. Taxonomic richness of all functional groups followed a unimodal relationship with water temperature, peaking at 23-25°C and declining below and above this relatively narrow thermal range. This suggests that relatively small changes in water temperature under expected future climate warming may alter taxonomic richness and ecological structure of these communities. Our findings improve the understanding of this unstudied but crucial component of bromeliad ecosystems and reveal important environmental filters that likely contribute to overall bromeliad community structure and function.