Search

Background: Post-radiation nasopharyngeal necrosis (PRNN) is a severe adverse event following re-radiotherapy for patients with locally recurrent nasopharyngeal carcinoma (LRNPC) and associated with decreased survival. Biological heterogeneity in recurrent tumors contributes to the different risks of PRNN. Radiomics can be used to mine high-throughput non-invasive image features to predict clinical outcomes and capture underlying biological functions. We aimed to develop a radiogenomic signature for the pre-treatment prediction of PRNN to guide re-radiotherapy in patients with LRNPC. Methods: This multicenter study included 761 re-irradiated patients with LRNPC at four centers in NPC endemic area and divided them into training, internal validation, and external validation cohorts. We built a machine learning (random forest) radiomic signature based on the pre-treatment multiparametric magnetic resonance images for predicting PRNN following re-radiotherapy. We comprehensively assessed the performance of the radiomic signature. Transcriptomic sequencing and gene set enrichment analyses were conducted to identify the associated biological processes. Results: The radiomic signature showed discrimination of 1-year PRNN in the training, internal validation, and external validation cohorts (area under the curve (AUC) 0.713–0.756). Stratified by a cutoff score of 0.735, patients with high-risk signature had higher incidences of PRNN than patients with low-risk signature (1-year PRNN rates 42.2–62.5% vs. 16.3–18.8%, P < 0.001). The signature significantly outperformed the clinical model (P < 0.05) and was generalizable across different centers, imaging parameters, and patient subgroups. The radiomic signature had prognostic value concerning its correlation with PRNN-related deaths (hazard ratio (HR) 3.07–6.75, P < 0.001) and all causes of deaths (HR 1.53–2.30, P < 0.01). Radiogenomics analyses revealed associations between the radiomic signature and signaling pathways involved in tissue fibrosis and vascularity. Conclusions: We present a radiomic signature for the individualized risk assessment of PRNN following re-radiotherapy, which may serve as a noninvasive radio-biomarker of radiation injury-associated processes and a useful clinical tool to personalize treatment recommendations for patients with LANPC. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze the imaging findings of 15 cases of malignant fibrous histiocytoma (MFH) of the head and neck, in order to better understand the tumor characteristics based on c omputed t omography (CT) and magnetic resonance imaging (MRI). CT (n=11) and MRI (n=4) images from 15 patients with histologically diagnosed MFH of the head and neck were retrospectively analyzed. The imaging characteristics were analyzed and compared among different histological subtypes. The lesions were primarily located in the maxillary sinus in 5 patients, the ethmoid sinus in 1 patient, the infratemporal fossa in 2 patients, the neck in 4 patients, the left mandible in 1 patient, the gingiva in 1 patient and the epiglottis in 1 patient. A total of 4 cases were associated with radiotherapy. All the lesions were ill-defined, ranging in size from 2.1 to 5.1 cm in the largest diameter. Bone fractures were evident in 9 cases. The attenuation, signal and enhancement patterns varied, although inflammatory MFH exhibited prolonged enhancement in dual-phase enhanced CT scans. MFH of the head and neck is rare but may be associated with radiotherapy. Although the imaging manifestations of MFH are various and non-specific, inflammatory MFH exhibits prolonged enhancement on dual-phase enhanced CT scans. [ABSTRACT FROM AUTHOR]

Theoretical investigation on particle transport in a 90 degree bend was carried out. The finite volume method was used to simulate the flow field in the bend pipe, and one-way coupled Lagrangian method was used to calculate the trajectory and deposition efficiency of microparticles. The unique relationship between the irreversible deposition efficiency and radius ratio of single-shell microparticle was given finally. [ABSTRACT FROM AUTHOR]

Previous studies have shown that patients with hepatitis B virus-related cirrhosis (HBVRC) without overt hepatic encephalopathy (OHE) are associated with a varying degree of cognitive dysfunction. Several resting-state functional magnetic resonance imaging (fMRI) studies have been conducted to explore the neural correlates of such cognitive deficits, whereas little effort has been made to investigate the cortical integrity in cirrhotic patients without OHE. Here, using cortical thickness, surface area and local gyrification index (lGI), this study performed a comprehensive analysis on the cortical morphometry of patients with HBV-RC without OHE (HBV-RC-NOHE) vs. matched healthy controls. Compared with healthy controls, we found significantly increased cortical thickness in the bilateral lingual and parahippocampal gyrus, right posterior cingulate cortex, precuneus, peri-calcarine sulcus and fusiform gyrus in patient with HBV-RC-NOHE, which may closely relate to be the low-grade brain edema. Cortical gyrification analysis showed significantly increased lGI in the left superior and inferior parietal cortex as well as lateral occipital cortex, which was speculated to be associated with disruptions in white matter connectivity and sub-optimal intra-cortical organization. In addition, the mean cortical thickness/lGI of the regions with structural abnormalities was shown to be negatively correlated with psychometric hepatic encephalopathy score (PHES) of the patients with HBV-RC-NOHE. These morphological changes may serve as potential markers for the preclinical diagnosis and progression of HBV-RC-NOHE. [ABSTRACT FROM AUTHOR]

Background ClC-3 channel/antiporter plays a critical role in a variety of cellular activities. ClC-3 has been detected in the ileum and colon. Objective To determine the functions of ClC-3 in the gastrointestinal tract. Design After administration of dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS), intestines from ClC-3-/- and wild-type mice were examined by histological, cellular, molecular and biochemical approaches. ClC-3 expression was determined by western blot and immunostaining. Results ClC-3 expression was reduced in intestinal tissues from patients with UC or Crohn's disease and from mice treated with DSS. Genetic deletion of ClC-3 increased the susceptibility of mice to DSS- or TNBS-induced experimental colitis and prevented intestinal recovery. ClC-3 deficiency promoted DSS-induced apoptosis of intestinal epithelial cells through the mitochondria pathway. ClC-3 interacts with voltage-dependent anion channel 1, a key player in regulation of mitochondria cytochrome c release, but DSS treatment decreased this interaction. In addition, lack of ClC-3 reduced the numbers of Paneth cells and impaired the expression of antimicrobial peptides. These alterations led to dysfunction of the epithelial barrier and invasion of commensal bacteria into the mucosa. Conclusions A defect in ClC-3 may contribute to the pathogenesis of IBD by promoting intestinal epithelial cell apoptosis and Paneth cell loss, suggesting that modulation of ClC-3 expression might be a new strategy for the treatment of IBD. [ABSTRACT FROM AUTHOR]