To identify patients who are likely to develop contrast-induced acute kidney injury (CI-AKI) in patients with acute myocardial infarction (AMI), a nomogram was developed in AMI patients. Totally 920 patients with AMI were enrolled in our study. The discrimination and calibration of the model were validated. External validations were also carried out in a cohort of 386 AMI patients. Our results showed in the 920 eligible AMI patients, 114 patients (21.3%) developed CI-AKI in the derivation group (n = 534), while in the validation set (n = 386), 50 patients (13%) developed CI-AKI. CI-AKI model included the following six predictors: hemoglobin, contrast volume >100 ml, hypotension before procedure, eGFR, log BNP, and age. The area under the curve (AUC) was 0.775 (95% confidence interval [CI]: 0.732–0.819) in the derivation group and 0.715 (95% CI: 0.631–0.799) in the validation group. The Hosmer-Lemeshow test has a p value of 0.557, which confirms the model’s goodness of fit. The AUC of the Mehran risk score was 0.556 (95% CI: 0.498–0.615) in the derivation group. The validated nomogram provided a useful predictive value for CI-AKI in patients with AMI.

As the most abundant nonprotein biothiol in living cells, glutathione (GSH) prevents cellular components from oxidative damage and maintains the intracellular redox homeostasis. For further exploring whether GSH can be employed as a bioindicator to discriminate tumor lesion at a cellular level, the highly selective detection and accurate quantification of GSH under pathological conditions are critical. Herein, we design a coumarin derivative-based two-photon fluorescent probe Cou-Br for the detection of GSH in living cells, mice models, and clinical specimens. The prepared probe is capable of sensitively and selectively detecting GSH in complex biological systems. Cou-Br displays a good linear relationship in response to GSH and a low limit of detection. With the fluorescence signal positively associated with intracellular GSH levels, the probe enables real-time imaging of GSH in various cell lines. Under the condition of CS 2 stimulation, Cou-Br can rapidly respond to the fluctuation of intracellular GSH induced by oxidative damage. Furthermore, the in situ and in vivo bioimaging performances of Cou-Br are demonstrated. Typically, relying on the different cellular concentrations of GSH, the probe is successfully employed to identify the human laryngeal cancer lesion with outstanding capabilities of deep tissue imaging and tumor margin recognition. We assume that the abnormal expression level of GSH may be utilized as a potential bioindicator to discriminate tumor tissues from the surrounding disease-free tissues. To conclude, the proposed probe Cou-Br may potentially serve as a powerful chemical tool for the surgical navigation of cancer in clinic.

Long non-coding RNAs (lncRNAs), a group of non-protein-coding RNAs longer than 200 nucleotides, are involved in multiple biological and pathological processes, such as proliferation, apoptosis, migration, invasion, angiogenesis, and immune escape. Many studies have shown that lncRNAs participate in the complex network of cancer and play vital roles as oncogenes or tumor-suppressor genes in a variety of cancers. Moreover, recent research has shown that abnormal expression of lncRNAs in malignant tumor cells before and after radiotherapy may participate in the progression of cancers and affect the radiation sensitivity of malignant tumor cells mediated by specific signaling pathways or cell cycle regulation. In this review, we summarize the published studies on lncRNAs in radiotherapy regarding the biological function and mechanism of human cancers, including esophageal cancer, pancreatic cancers, nasopharyngeal carcinoma, hepatocellular carcinoma, cervical cancer, colorectal cancer, and gastric cancer.

Long non-coding RNAs (lncRNAs) have been demonstrated to be critical regulators in tumorigenesis. LncRNA SPRY4-IT1 has been identified as critical regulator for hepatocellular carcinoma and ovarian cancer. However, the potential role and clinical value of SPRY4-IT1 in human thyroid cancer (TC) still remain unclear and need to be uncovered. Our current study was aimed to ascertain the biological role of expression of SPRY4-IT1 in TC tissues and cells. Our findings revealed that the level of SPRY4-IT1 was significantly upregulated in TC tissues and cell lines, which was correlated with poor prognosis. And cellular experiments exhibited that silenced SPRY4-IT1 inhibited the proliferative and migratory abilities of TC cells. Mechanism assays noted that silenced SPRY4-IT1 could increase the levels of transforming growth factor-β1 (TGF-β1) and p-Smad2/3 and function mediated by si-SPRY4-IT1 could be rescued by the interference of TGF-β1. Generally speaking, these findings elucidated that SPRY4-IT1 might become a novel prognostic factor in the clinical behaviors of TC patients and participated in the progression of TC through targeting TGF-β/Smad signaling pathway.