Development of a combined model incorporating clinical characteristics and magnetic resonance imaging features to enhance the predictive value of a prognostic model for locally advanced cervical cancer

ObjectiveThis study aimed to develop non-invasive predictive tools based on clinical characteristics and magnetic resonance imaging (MRI) features to predict survival in patients with locally advanced cervical cancer (LACC), thereby facilitating clinical decision-making.MethodsWe conducted a retrospective analysis of clinical and MRI data from LACC patients who underwent radical radiotherapy at our center between September 2012 and May 2020. Prognostic predictors were identified using single-factor and multifactor Cox analyses. Clinical and MRI models were established based on relevant features, and combined models were created by incorporating MRI factors into the clinical model. The predictive performance of the models was evaluated using the area under the curve (AUC), consistency index (C-index), and decision curve analysis (DCA).ResultsThe study included 175 LACC patients. Multivariate Cox analysis revealed that patients with FIGO IIA-IIB stage, ECOG score 0-1, CYFRA 21-1<7.7 ng/ml, ADC ≥ 0.79 mm^2/s, and Kep ≥ 4.23 minutes had a more favorable survival prognosis. The clinical models, incorporating ECOG, FIGO staging, and CYFRA21-1, outperformed individual prognostic factors in predicting 5-year overall survival (AUC: 0.803) and 5-year progression-free survival (AUC: 0.807). The addition of MRI factors to the clinical model (AUC: 0.803 for 5-year overall survival) increased the AUC of the combined model to 0.858 (P=0.011). Similarly, the combined model demonstrated a superior predictive ability for 5-year progression-free survival, with an AUC of 0.849, compared to the clinical model (AUC: 0.807) and the MRI model (AUC: 0.673). Furthermore, the C-index of the clinical models for overall survival and progression-free survival were 0.763 and 0.800, respectively. Upon incorporating MRI factors, the C-index of the combined model increased to 0.826 for overall survival and 0.843 for progression-free survival. The DCA further supported the superior prognostic performance of the combined model.ConclusionOur findings indicate that ECOG, FIGO staging, and CYFRA21-1 in clinical characteristics, as well as ADC and Kep values in MRI features, are independent prognostic factors for LACC patients undergoing radical radiotherapy. The combined models provide enhanced predictive ability in assessing the risk of patient mortality and disease progression

The complete mitochondrial genome of Reticulitermes leptomandibularis (Isoptera: Rhinotermitidae)

The complete mitochondrial genome of a lower termite, Reticulitermes leptomandibularis is a typical circular DNA molecule of 15,920 bp in length. The genome contains 13 protein-coding genes (PCGs), 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes, and a non-coding region (D-loop).The overall sequence of R. leptomandibularis is A/T biased with a percentage of 65.36%. The phylogenetic tree constructed using complete mitochondrial genomes of Reticulitermes genus revealed that R. leptomandibularis was closest to Reticulitermes aculabialis and formed a sister group to Reticulitermes speratus. This whole mt genome provides molecular resource for evolution analysis within termites especially the genus Reticulitermes

Exposure to ambient particulate matter alters the microbial composition and induces immune changes in rat lung

Abstract Background Ambient particulate matter exposure has been shown to increase the risks of respiratory diseases. However, the role of the lung microbiome and the immune response to inhaled particulate matter are largely unexplored. We studied the influence of biomass fuel and motor vehicle exhaust particles on the lung microbiome and pulmonary immunologic homeostasis in rats. Methods Fifty-seven Sprague–Dawley rats were randomly divided into clean air (CON), biomass fuel (BMF), and motor vehicle exhaust (MVE) groups. After a 4-week exposure, the microbial composition of the lung was assessed by 16S rRNA pyrosequencing, the structure of the lung tissue was assessed with histological analysis, the phagocytic response of alveolar macrophages to bacteria was determined by flow cytometry, and immunoglobulin concentrations were measured with commercial ELISA kits. Results There was no significant difference in lung morphology between the groups. However, the BMF and MVE groups displayed greater bacterial abundance and diversity. Proteobacteria were present in higher proportions in the MVE group, and 12 bacterial families differed in their relative abundances between the three groups. In addition, particulate matter exposure significantly increased the capacity of alveolar macrophages to phagocytose bacteria and induced changes in immunoglobulin levels. Conclusion We demonstrated that particulate matter exposure can alter the microbial composition and change the pulmonary immunologic homeostasis in the rat lung

Nicotine-Induced Airway Smooth Muscle Cell Proliferation Involves TRPC6-Dependent Calcium Influx Via α7 nAChR

Background/Aims: The proliferation of human bronchial smooth muscle cells (HBSMCs) is a key pathophysiological component of airway remodeling in chronic obstructive pulmonary disease (COPD) for which pharmacotherapy is limited, and only slight improvements in survival have been achieved in recent decades. Cigarette smoke is a well-recognized risk factor for COPD; however, the pathogenesis of cigarette smoke-induced COPD remains incompletely understood. This study aimed to investigate the mechanisms by which nicotine affects HBSMC proliferation. Methods: Cell viability was assessed with a CCK-8 assay. Proliferation was measured by cell counting and EdU immunostaining. Fluorescence calcium imaging was performed to measure intracellular Ca2+ concentration ([Ca2+]i). Results: The results showed that nicotine promotes HBSMC proliferation, which is accompanied by elevated store-operated calcium entry (SOCE), receptor-operated calcium entry (ROCE) and basal [Ca2+]i in HBSMCs. Moreover, we also confirmed that canonical transient receptor potential protein 6 (TRPC6) and α7 nicotinic acetylcholine receptor (α7 nAChR) are involved in nicotine-induced upregulation of cell proliferation. Furthermore, we verified that activation of the PI3K/Akt signaling pathway plays a pivotal role in nicotine-enhanced proliferation and calcium influx in HBSMCs. Inhibition of α7 nAChR significantly decreased Akt phosphorylation levels, and LY294002 inhibited the protein expression levels of TRPC6. Conclusion: Herein, these data provide compelling evidence that calcium entry via the α7 nAChR-PI3K/Akt-TRPC6 signaling pathway plays an important role in the physiological regulation of airway smooth muscle cell proliferation, representing an important target for augmenting airway remodeling