Multimodality US versus Thyroid Imaging Reporting and Data System Criteria in Recommending Fine-Needle Aspiration of Thyroid Nodules.

Background Current guidelines recommend the use of conventional US for risk stratification and management of thyroid nodules. However, fine-needle aspiration (FNA) is often recommended in benign nodules. Purpose To compare the diagnostic performance of multimodality US (including conventional US, strain elastography, and contrast-enhanced US [CEUS]) with the American College of Radiology Thyroid Imaging Reporting and Data System (TI-RADS) in the recommendation of FNA for thyroid nodules to reduce unnecessary biopsies. Materials and Methods In this prospective study, 445 consecutive participants with thyroid nodules from nine tertiary referral hospitals were recruited between October 2020 and May 2021. With univariable and multivariable logistic regression, the prediction models incorporating sonographic features, evaluated with interobserver agreement, were constructed and internally validated with bootstrap resampling technique. In addition, discrimination, calibration, and decision curve analysis were performed. Results A total of 434 thyroid nodules confirmed at pathologic analysis (259 malignant thyroid nodules) in 434 participants (mean age, 45 years ± 12 [SD]; 307 female participants) were included. Four multivariable models incorporated participant age, nodule features at US (proportion of cystic components, echogenicity, margin, shape, punctate echogenic foci), elastography features (stiffness), and CEUS features (blood volume). In recommending FNA in thyroid nodules, the highest area under the receiver operating characteristic curve (AUC) was 0.85 (95% CI: 0.81, 0.89) for the multimodality US model, and the lowest AUC was 0.63 (95% CI: 0.59, 0.68) for TI-RADS (P < .001). At the 50% risk threshold, 31% (95% CI: 26, 38) of FNA procedures could be avoided with multimodality US compared with 15% (95% CI: 12, 19) with TI-RADS (P < .001). Conclusion Multimodality US had better performance in recommending FNA to avoid unnecessary biopsies than the TI-RADS. Clinical trial registration no. NCT04574258 © RSNA, 2023 Supplemental material is available for this article.

Congenital absence of left atrial appendage in a patient with ischemic stroke and atrial fibrillation.

Left atrial appendage (LAA) is a finger-like muscular extension of the left atrium, and it is the most prominent site for cardiac thrombus in patients with atrial fibrillation. Congenital absence of LAA could be incidentally detected in patient with ischemic stroke and atrial fibrillation. Although it is considered to be an extremely rare cardiac anomaly, its clinical significance remains unknown and there is no clear consensus in the management strategy in those patients. Therefore, we report a case of an incidentally noted congenital absence of LAA in a 68-year-old woman being planned for LAA closure.

Unicentric Castleman disease was misdiagnosed as pancreatic mass: A case report.

BACKGROUND: Castleman's disease (CD) is a lymphatic proliferative disorder of unknown cause and is rarely seen clinically. It has been divided into unicentric and multicentric types. Unicentric CD (UCD) occurs as a solitary enlarged mass and mediastinal lymph nodes are the most common site. Surgical excision has proven to be curative for UCD. Multicentric CD (MCD) appears as a systemic disease with peripheral lymphadenopathy. MCD had a poor response to surgery and monoclonal antibodies with rituximab have become a research hotspot. CASE SUMMARY: A 44-year-old woman presented with a pancreatic mass during routine physical examination. She had no obvious symptoms, such as fever, abdominal pain, abdominal distension, or jaundice. Ultrasound examination indicated a hypoechoic mass between the body of the pancreas, left lobe of the liver and stomach. It had a clear boundary, irregular shape, uneven echo, and no obvious blood flow signals. To clarify the diagnosis, contrast-enhanced ultrasound examination was performed, which showed a benign pancreatic lesion. Neuroendocrine or solid pseudopapillary tumor was a possible diagnosis. The patient underwent further contrast-enhanced computed tomography and contrast-enhanced magnetic resonance imaging, which were suggestive of solid pseudopapillary tumor or neuroendocrine tumor. All the examinations failed to give a definitive diagnosis, and the patient underwent surgery. The final pathological and immunohistochemical results showed that the mass was CD. CONCLUSION: This case highlights when lymphadenopathy is encountered clinically, CD should be considered and a biopsy should be performed.

Diosgenin inhibits angiotensin II-induced extracellular matrix remodeling in cardiac fibroblasts through regulating the TGF­ß1/Smad3 signaling pathway.

The proliferation of cardiac fibroblasts (CFs) and deposition of extracellular matrix (ECM) proteins are pivotal in the development of cardiac fibrosis. Recent studies have indicated that diosgenin may inhibit high glucose­induced renal tubular fibrosis; however, to the best of our knowledge, no studies have focused on the effects of diosgenin on cardiac fibrosis. Therefore, the present study aimed to explore the effects of diosgenin on angiotensin II (Ang II)­induced ECM remodeling, and its possible mechanism in rat CFs. CFs were pre­incubated with diosgenin (1, 5 and 10 µM) for 24 h and were then stimulated with Ang II (100 nM) for 24 h. Cell proliferation was estimated using the MTS assay. The expression levels of α­SMA, fibronectin, collagen I, TGF­ß1, in addition to phosphorylation of Smad3 were detected by western blotting. The results demonstrated that diosgenin inhibited Ang II­induced CF proliferation and the differentiation of CFs to myofibroblasts. In addition, diosgenin was able to inhibit Ang II­induced ECM expression in rat CFs. Furthermore, diosgenin inhibited Ang II­induced expression of transforming growth factor­ß1 (TGF­ß1) and Smad3 phosphorylation in CFs. Taken together, these results suggest that diosgenin may inhibit Ang II­induced ECM remodeling by suppressing the TGF­ß1/Smad3 signaling pathway in rat CFs. Therefore, diosgenin may possess therapeutic potential for the treatment of cardiac fibrosis.

Inhibiting High-Mobility Group Box 1 (HMGB1) Attenuates Inflammatory Cytokine Expression and Neurological Deficit in Ischemic Brain Injury Following Cardiac Arrest in Rats.

Cardiac arrest (CA), if untreated for more than 5 min, can induce severe brain damage, the underlying mechanism of which is still unclear. Previous studies have indicated that high-mobility group box 1 (HMGB1), a nuclear protein implicated in several inflammatory disorders, is involved in the inflammatory processes following brain ischemia. However, the role of HMGB1 in brain dysfunction after CA is yet to be determined. In a rat CA model, HMGB1 protein expression was higher at 1, 3, and 7 days post-CA, compared to that in naïve and sham-treated rats. Following injection of HMGB1 antibody (anti-HMGB1) into the cerebral ventricles, neurological deficit scores were significantly decreased in the CA group as compared to that in the naïve and sham group. Nissl staining showed significant neuronal loss in the hippocampal CA1 region following CA, which was significantly attenuated by anti-HMGB1-treatment (10 and 50 µg) in comparison with the vehicle-injected control. CA induced a significant increase in the levels of the cytokine interleukin-1ß (IL-1ß) and tumor necrosis factor α (TNF-α) in the hippocampus as revealed by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Treatment with anti-HMGB1 significantly inhibited IL-1ß and TNF-α expression. Our study suggests that HMGB1 contributes significantly to CA-induced brain dysfunction and that inhibiting HMGB1 function and expression may be an effective therapeutic approach to CA-induced ischemic brain injury.

Pulmonary valve endocarditis associated with a ruptured aneurysm of the right sinus of Valsalva.

Pulmonary valve endocarditis is an extremely rare complication of aneurysm of the sinus of Valsalva. We report the case of a 26-year-old male patient who presented with pulmonary valve endocarditis which was associated with a ruptured aneurysm of the right sinus of Valsalva with aorto-right ventricular outflow tract fistula and aortic valve endocarditis. He underwent aortic valve replacement with a 23 mm pericardial bioprosthesis, reconstruction of the right sinus of Valsalva using a pericardial patch, and debridement of pulmonary valve leaflet vegetations. The operation was a complete success. Intraoperative transesophageal echocardiography showed no residual shunt within the reconstructed right coronary sinus, normal function of aortic bioprosthesis, and mild mitral, tricuspid, and pulmonary regurgitation. Postoperative antibiotics were continued and the patient recovered uneventfully.