No abstract

CMBs is a common radiological manifestation in NPC patients with RN. The number of temporal CMBs is independently associated with increased likelihood of cognitive dysfunction in patients with RN.

Radiation-induced brachial plexopathy (RIBP) is one of the late complications in nasopharyngeal carcinoma (NPC) patients who received radiotherapy. We conducted a retrospective study to investigate its clinical characteristics and risk factors. Thirty-onepatients with RIBP after radiotherapy for NPC were enrolled. Clinical manifestations of RIBP, electrophysiologic data, magnetic resonance imaging (MRI), and the correlation between irradiation strategy and incidence of RIBP were evaluated. The mean latency at the onset of RIBP was 4.26 years. Of the symptoms, paraesthesia usually presented first (51.6%), followed by pain (22.6%) and weakness (22.6%). The major symptoms included paraesthesia (90.3%), pain (54.8%), weakness (48.4%), fasciculation (19.3%) and muscle atrophy (9.7%). Nerve conduction velocity (NCV) and electromyography (EMG) disclosed that pathological changes of brachial plexus involved predominantly in the upper and middle trunks in distribution. MRI of the brachial plexus showed hyper-intensity on T1, T2, post-contrast T1 and diffusion weighted whole body imaging with background body signal suppression (DWIBS) images in lower cervical nerves. Radiotherapy with Gross Tumor volume (GTVnd) and therapeutic dose (mean 66.8±2.8Gy) for patients with lower cervical lymph node metastasis was related to a significantly higher incidence of RIBP (P<0.001). Thus, RIBP is a severe and progressive complication of NPC after radiotherapy. The clinical symptoms are predominantly involved in upper and middle trunk of the brachial plexus in distribution. Lower cervical lymph node metastasis and corresponding radiotherapy might cause a significant increase of the RIBP incidence.

In recent years, LNK, an adapter protein, has been found to be associated with metabolic diseases, including hypertension and diabetes. We found that the expression of LNK in human adipose tissue was positively correlated with serum glucose and insulin in obese people. We examined the role of LNK in insulin resistance and systemic energy metabolism using LNK-deficient mice ( LNK -/- ). With consumption of a high-fat diet, wild type (WT) mice accumulated more intrahepatic triglyceride, higher serum triglyceride (TG), free fatty acid (FFA) and high sensitivity C-reactive protein (hsCRP) compared with LNK -/- mice. However, there was no significant difference between LNK -/- and WT mice under normal chow diet. Meanwhile, glucose transporter 4 (GLUT4) expression in adipose tissue and insulin-stimulated glucose uptake in adipocytes were increased in LNK -/- mice. LNK -/- adipose tissue showed activated reactivity for IRS1/PI3K/Akt/AS160 signaling, and administration of a PI3K inhibitor impaired glucose uptake. In conclusion, LNK plays a pivotal role in adipose glucose transport by regulating insulin-mediated IRS1/PI3K/Akt/AS160 signaling.

No abstract

Inflammatory myofibroblastic tumor (IMT) is an unusual tumor composed of differentiated myofibroblastic spindle cells usually accompanied by numerous plasma cells and lymphocytes. IMT was originally described in the lung; occurrence in a long bone is rare. We present two examples of IMT arising in a long bone: one in the humerus and one in the femur. In both cases, imaging shows a poorly delineated osteolytic lesion with cortical bone destruction that aggressively extends into surrounding soft tissue. Histologically, the lesion is dominated by differentiated spindle cells with aprominent collagenous stroma and an inflammatory component including plasma cells and lymphocytes, and with positive immunoreactivity for anaplastic lymphoma kinase. The absence of cytologic atypia helps differentiate this lesion from malignant spindle cell tumors.

Background: Due to the uncertainty of the success of percutaneous coronary intervention (PCI) and the complexity of selecting suitable treatment cases, the interventional outcome of coronary chronic total occlusion (CTO) remains challenging. The purpose of this study was to evaluate the role of quantitative plaque analysis based on coronary computed tomography angiography (CCTA) in predicting the CTO-PCI outcome. Methods: We retrospectively included 78 patients with CTO (80 lesions) confirmed by invasive coronary angiography from July 2016 to December 2018. All patients underwent PCI treatment according to standard practice. A total of 47 lesions in 47 patients were successfully treated with PCI. PCI failed in the remaining 33 lesions in 31 patients. The following conventional CCTA morphologic parameters were evaluated and compared between the PCI-success and PCI-failure groups: stump morphology; occlusion length, tortuous course; CTO lesion calcium; bridging collateral vessel; retrograde collateral vessel; the appearance of the occluded distal segment; and quantitative CTO plaque characteristics, including total plaque volume, calcified plaque (CP) volume, noncalcified plaque (NCP) volume, low-density noncalcified plaque (LDNCP) volume, and plaque length. Univariate and multivariate logistic regression analyses were performed to determine independent parameters predictive of CTO-PCI outcomes. The predictive performances were assessed using receiver operating characteristic curve analysis. Results: The blunt stump was the only independent CCTA morphologic parameter to predict the outcome of CTO-PCI [odds ratio (OR): 10.807; P<0.001]. NCP volume (OR: 1.018; P<0.001), CP volume (OR: 1.026; P=0.049), and plaque length (OR: 1.058; P=0.037) were independent quantitative CTO plaque characteristics predictive of CTO-PCI outcomes. The plaque-based model combining NCP volume with CP volume and plaque length had a higher area under the curve (AUC 0.96) than did the morphology-based model that

Objectives Whether a stenosis can cause hemodynamic lesion-specific ischemia is critical for the treatment decision in patients with coronary artery disease (CAD). Based on coronary computed tomography angiography (CCTA), CT fractional flow reserve (FFRCT) can be used to assess lesion-specific ischemia. The selection of an appropriate site along the coronary artery tree is vital for measuring FFRCT. However the optimal site to measure FFRCT for a target stenosis remains to be adequately determined. The purpose of this study was to determine the optimal site to measure FFRCT for a target lesion in detecting lesion-specific ischemia in CAD patients by evaluating the performance of FFRCT measured at different sites distal to the target lesion in detecting lesion-specific ischemia with FFR measured with invasive coronary angiography (ICA) as reference standard. Methods In this single-center retrospective cohort study, a total of 401 patients suspected of having CAD underwent invasive ICA and FFR between March 2017 and December 2021 were identified. 52 patients having both CCTA and invasive FFR within 90 days were enrolled. Patients with vessels 30%-90% diameter stenosis as determined by ICA were referred to invasive FFR evaluation, which was performed 2–3 cm distal to the stenosis under the condition of hyperemia. For each vessel with 30%–90% diameter stenosis, if only one stenosis was present, this stenosis was selected as the target lesion; if serial stenoses were present, the stenosis most distal to the vessel end was chosen as the target lesion. FFRCT was measured at four sites: 1 cm, 2 cm, and 3 cm distal to the lower border of the target lesion (FFRCT-1 cm, FFRCT-2 cm, FFRCT-3 cm), and the lowest FFRCT at the distal vessel tip (FFRCT-lowest). The normality of quantitative data was assessed using the Shapiro–Wilk test. Pearson's correlation analysis and Bland–Altman plots were used for assessing the correlation and difference between invasive FFR and FFRCT. Correlation coefficients derived from Chi-suqare test were used to assess the correlation between invasive FFR and the cominbaiton of FFRCT measred at four sites. The performances of significant obstruction stenosis (diameter stenosis ≥ 50%) at CCTA and FFRCT measured at the four sites and their combinations in diagnosing lesion-specific ischemia were evaluated by receiver-operating characteristic (ROC) curves using invasive FFR as the reference standard. The areas under ROC curves (AUCs) of CCTA and FFRCT were compared by the DeLong test. Results A total of 72 coronary arteries in 52 patients were included for analysis. Twenty-five vessels (34.7%) had lesion-specific ischemia detected by invasive FFR and 47 vesseles (65.3%) had no lesion-spefifice ischemia. Good correlation was found between invasive FFR and FFRCT-2 cm and FFRCT-3 cm (r = 0.80, 95% CI, 0.70 to 0.87, p < 0.001; r = 0.82, 95% CI, 0.72 to 0.88, p < 0.001). Moderate correlation was found between invasive FFR and FFRCT-1 cm and FFRCT-lowest (r = 0.77, 95% CI, 0.65 to 0.85, p < 0.001; r = 0.78, 95% CI, 0.67 to 0.86, p < 0.001). FFRCT-1 cm + FFRCT-2 cm, FFRCT-2 cm + FFRCT-3 cm, FFRCT-3 cm + FFRCT-lowest, FFRCT-1 cm + FFRCT-2 cm + FFRCT-3 cm, and FFRCT-2 cm + FFRCT-3 cm + FFRCT-lowest were correatled with invasive FFR (r = 0.722; 0.722; 0.701; 0.722; and 0.722, respectively; p < 0.001 for all). Bland–Altman plots revealed a mild difference between invasive FFR and the four FFRCT (invasive FFR vs. FFRCT-1 cm, mean difference -0.0158, 95% limits of agreement: -0.1475 to 0.1159; invasive FFR vs. FFRCT-2 cm, mean difference 0.0001, 95% limits of agreement: -0.1222 to 0.1220; invasive FFR vs. FFRCT-3 cm, mean difference 0.0117, 95% limits of agreement: -0.1085 to 0.1318; and invasive FFR vs. FFRCT-lowest, mean difference 0.0343, 95% limits of agreement: -0.1033 to 0.1720). AUCs of CCTA, FFRCT-1 cm, FFRCT-2 cm, FFRCT-3 cm, and FFRCT-lowest in detecting lesion-specific ischemia were 0.578, 0.768, 0.857, 0.856 and 0.770, respectively. All FFRCT had a higher AUC than CCTA (all p < 0.05), FFRCT-2 cm achieved the highest AUC at 0.857. The AUCs of FFRCT-2 cm and FFRCT-3 cm were comparable (p > 0.05). The AUCs were similar between FFRCT-1 cm + FFRCT-2 cm, FFRCT-3 cm + FFRCT-lowest and FFRCT-2 cm alone (AUC = 0.857, 0.857, 0.857, respectively; p > 0.05 for all). The AUCs of FFRCT-2 cm + FFRCT-3 cm, FFRCT-1 cm + FFRCT-2 cm + FFRCT-3 cm, FFRCT-and 2 cm + FFRCT-3 cm + FFRCT-lowest (0.871, 0.871, 0.872, respectively) were slightly higher than that of FFRCT-2 cm alone (0.857), but without significnacne differences (p > 0.05 for all). Conclusions FFRCT measured at 2 cm distal to the lower border of the target lesion is the optimal measurement site for identifying lesion-specific ischemia in patients with CAD.