Background: Tumor-associated macrophages (TAMs) are classified into two major phenotypes, M1 and M2. M1 TAMs suppress cancer progression, while M2 TAMs promote it. However, little is known regarding the role of TAMs in the development of ovarian cancer. Here, we investigated the relationship between TAM distribution patterns (density, microlocalization, and differentiation) and ovarian cancer histotypes, and we explored whether altered TAM distribution patterns influence long-term outcomes in ovarian cancer patients. Methods: A total of 112 ovarian cancer patients were enrolled in this study, and the subjects were divided into two groups according to their survival (< 5 years vs. ≥ 5 years). Immunohistochemistry and immunofluorescence were used to determine the density, microlocalization, and differentiation status of TAMs in ovarian cancer tissues for each histotype. Kaplan-Meier survival and multivariate Cox regression analyses were used to evaluate the prognostic significance of TAM-related parameters in ovarian cancer.

Integrating various enzymes with nanomaterials provides various nanohybrids with new possibilities in biosensor applications. Furthermore, the enzymatic activity and stability are also improved due to the large surface area of nanomaterials. Here we report the conjugation of glucose oxidase (GOD) onto phosphorescent Mn-doped ZnS quantum dots (QDs) using 1-ethyl-3-(3-dimethylaminopropy)carbodiimide (EDC)/N-hydroxysuccinimide (NHS) as coupling reagents for glucose biosensing based on the effective quenching of the room temperature phosphorescence (RTP) of Mn-doped ZnS QDs by the H(2)O(2) generated from GOD-catalyzed oxidation of glucose. The obtained bioconjugate not only provided improved enzymatic performance with Michaelis-Menten constant of 0.70 mM but also favored biological applications because the phosphorescent detection mode avoided the interference from autofluorescence and scattering light from the biological matrix. In addition, the GOD-conjugated Mn-doped ZnS QDs showed better thermal stability in the temperature range of 20-80 degrees C. The GOD-Mn-doped ZnS QDs based RTP sensor for glucose gave a detection limit of 3 microM and two linear ranges from 10 microM to 0.1 mM and from 0.1 to 1 mM. The developed biosensor was successfully applied to the determination of glucose in real serum samples without the need for any complicated sample pretreatments.

While most research works focus on the development of quantum dots (QDs)-based fluorescence sensors, much less attention is paid to the phosphorescence properties of QDs and their potential for phosphorescence detection. In this work, the phosphorescence property of Mn-doped ZnS QDs is explored to develop a novel room-temperature phosphorescence (RTP) method for the facile, rapid, cost-effective, sensitive, and selective detection of enoxacin in biological fluids. The Mn-doped ZnS QDs-based RTP method reported here does not need the use of deoxidants and other inducers and allows the detection of enoxacin in biological fluids without interference from autofluorescence and the scattering light of the matrix. The Mn-doped ZnS QDs offer excellent selectivity for detecting enoxacin in the presence of the main relevant metal ions in biological fluids, biomolecules, and other kinds of antibiotics. Quenching of the phosphorescence emission due to the addition of enoxacin at 1.0 microM is unaffected by 5000-fold excesses of Na (+) and 10000-fold excesses of K (+), Mg (2+), and Ca (2+). Amino acids such as tryptophan, histidine, and l-cysteine at 1000-fold concentration of enoxacin do not affect the detection of enoxacin. Glucose does not affect the detection at 10000-fold concentration of enoxacin. Typical coadministers (mainly other types of antibiotics) such as ceftezole, cefoperazone, oxacillin, and kalii dehydrographolidi succinas are permitted at 50-, 10-, 100-, and 50-fold excesses, respectively, without interference with the detection of enoxacin. The precision for 11 replicate detections of 0.4 microM enoxacin is 1.8% (RSD). The detection limit for enoxacin is 58.6 nM. The recovery of spiked enoxacin in human urine and serum samples ranges from 94 to 104%. The developed Mn-doped ZnS QDs-based RTP method is employed to monitor the time-dependent concentration of enoxacin in urine from a healthy volunteer after the oral medication of enoxacin. The investigation provides evidence that doped QDs are promising for RTP detection in further applications.

Purpose: We aimed to characterize the role of selenium-binding protein 1 (SBP1) in hepatocellular carcinoma (HCC) invasiveness and underlying clinical significance.Experimental Design: SBP1 expression was measured in stepwise metastatic HCC cell lines by Western blotting. The role of SBP1 in HCC was investigated using siRNA. Immunofluorescence analyses were used to detect the interaction between SBP1 and glutathione peroxidase 1 (GPX1). Nineteen fresh tumor tissues and 323 paraffin-embedded samples were used to validate in vitro findings and to detect the prognostic significance of SBP1, respectively.Results: Inhibition of SBP1 effectively increased cell motility, promoted cell proliferation, and inhibited apoptosis only under oxidative stress; it also greatly enhanced GPX1 activity without altering GPX1 expression and downregulated hypoxia-inducible factor-1a (HIF-1a) expression. SBP1 and GPX1 formed nuclear bodies and colocalized under oxidative stress. In freshly isolated clinical HCC tissues, decreased SBP1 was linked with increased GPX1 activity and correlated with vascular invasion. Tumor tissue microarrays indicated that SBP1 was an independent risk factor for overall survival and disease recurrence; patients with lower SBP1 expression experienced shorter overall survival periods and higher rates of disease recurrence (P < 0.001). Further analyses indicated that the predictive power of SBP1 was more significant for patients beyond the Milan criteria than patients within the Milan criteria.Conclusions: Decreased expression of SBP1 could promote tumor invasiveness by increasing GPX1 activity and diminishing HIF-1a expression in HCC; SBP1 could be a novel biomarker for predicting prognosis and guiding personalized therapeutic strategies, especially in patients with advanced HCC.