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A Zn(II) coordination polymer (CP), namely, {[Zn(DTPB)]·DMF}n (H2DTPB = 1-(3,5-di(2H-tetrazol-5-yl)phenyl)-1H-benzeimidazole, Zn-DTPB), was assembled from a new tetrazolyl–benzimidazolyl heterotopic triangular ligand. In Zn-DTPB, the tetrazolyl groups connect the Zn(II) ions into a 2D network with a (4·82) topology, and the 2D network is further interconnected by Zn–N bonds between Zn(II) and benzimidazolyl groups to a 3D framework featuring a 4-connected sra topology. The DMF molecules were tightly encapsulated in the framework and could not be released until the framework decomposed. The framework is stable up to 300 °C and can be retained in water for 72 h. The luminescence in the solid-state and in various solvents was investigated, implying that Zn-DTPB can be used to detect acetone and triethylamine (TEA) in water by fluorescence quenching with good sensitivity and selectivity. Moreover, Zn-DTPB exhibited excellent reproducibility in sensing acetone. Mechanistic studies have shown that the fluorescence quenching of acetone and triethylamine is caused by competitive absorption and structural amorphization, respectively. Interestingly, the amorphous product can be transformed into Zn-DTPB crystals through a solvent-media structural transformation process. [ABSTRACT FROM AUTHOR]

Background: Prostate cancer is a significant clinical issue, particularly for high Gleason score (GS) malignancy patients. Our study aimed to engineer and validate a risk model based on the profiles of high-GS PCa patients for early identification and the prediction of prognosis. Methods: We conducted differential gene expression analysis on patient samples from The Cancer Genome Atlas (TCGA) and enriched our understanding of gene functions. Using the least absolute selection and shrinkage operator (LASSO) regression, we established a risk model and validated it using an independent dataset from the International Cancer Genome Consortium (ICGC). Clinical variables were incorporated into a nomogram to predict overall survival (OS), and machine learning was used to explore the risk factor characteristics' impact on PCa prognosis. Our prognostic model was confirmed using various databases, including single-cell RNA-sequencing datasets (scRNA-seq), the Cancer Cell Line Encyclopedia (CCLE), PCa cell lines, and tumor tissues. Results: We identified 83 differentially expressed genes (DEGs). Furthermore, WASIR1, KRTAP5-1, TLX1, KIF4A, and IQGAP3 were determined to be significant risk factors for OS and progression-free survival (PFS). Based on these five risk factors, we developed a risk model and nomogram for predicting OS and PFS, with a C-index of 0.823 (95% CI, 0.766–0.881) and a 10-year area under the curve (AUC) value of 0.788 (95% CI, 0.633–0.943). Additionally, the 3-year AUC was 0.759 when validating using ICGC. KRTAP5-1 and WASIR1 were found to be the most influential prognosis factors when using the optimized machine learning model. Finally, the established model was interrelated with immune cell infiltration, and the signals were found to be differentially expressed in PCa cells when using scRNA-seq datasets and tissues. Conclusions: We engineered an original and novel prognostic model based on five gene signatures through TCGA and machine learning, providing new insights into the risk of scarification and survival prediction for PCa patients in clinical practice. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) is a critical global public health issue with its incidence on the rise. Radiation therapy holds a primary role in PCa treatment; however, radiation resistance has become increasingly challenging as we uncover more about PCa's pathogenesis. Our review aims to investigate the multifaceted mechanisms underlying radiation therapy resistance in PCa. Specifically, we will examine how various factors, such as cell cycle regulation, DNA damage repair, hypoxic conditions, oxidative stress, testosterone levels, epithelial–mesenchymal transition, and tumor stem cells, contribute to radiation therapy resistance. By exploring these mechanisms, we hope to offer new insights and directions towards overcoming the challenges of radiation therapy resistance in PCa. This can also provide a theoretical basis for the clinical application of novel ultra-high-dose-rate (FLASH) radiotherapy in the era of PCa. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the potential clinical benefits of using stereotactic body radiation therapy (SBRT) with simultaneous integrated boost (SIB) technique for locally advanced pancreatic cancer (LAPC) among different treatment modalities and planning strategies, including photon and proton. Method: A total of 19 patients were retrospectively selected in this study: 13 cases with the tumor located in the head of the pancreas and 6 cases with the tumor in the body of the pancreas. SBRT-SIB plans were generated using volumetric modulated arc therapy (VMAT), two-field Intensity Modulated Proton Therapy (IMPT), and three-field IMPT. The IMPT used the robust optimization parameters of ± 3.5% range and 5-mm setup uncertainties. Root-mean-square deviation dose (RMSD) volume histograms were used to evaluate the target coverage robustness quantitatively. Dosimetric metrics based on the dose-volume histogram (DVH), homogeneity index (HI), and normal tissue complication probability (NTCP) were analyzed to evaluate the potential clinical benefits among different planning groups. Results: With a similar CTV and SIB coverage, two-field IMPT provided a lower maximum dose for the stomach (median: 18.6GyE, p<0.05) and duodenum (median: 32.62GyE, p<0.05) when the target was located in the head of the pancreas compared to VMAT and three-field IMPT. The risks of gastric bleed (3.42%) and grade ≥ 3 GI toxicity (4.55%) were also decreased. However, for the target in the body of the pancreas, VMAT showed a lower maximum dose for the stomach (median 30.93GyE, p<0.05) and toxicity of gastric bleed (median: 8.67%, p<0.05) compared to two-field IMPT and three-field IMPT, while other maximum doses and NTCPs were similar. The RMSD volume histogram (RVH) analysis shows that three-field IMPT provided better robustness for targets but not for OARs. Instead, three-field IMPT increased the Dmean of organs such as the stomach, duodenum, and intestine. Conclusion: The results indicated that the tumor locations could play a critical role in determining clinical benefits among different treatment modalities. Two-field IMPT could be a better option for LAPC patients whose tumors are located in the head of the pancreas. It provides lower severe toxicity for the stomach and duodenum. Nevertheless, VMAT is preferred for the body with better protection for the possibility of gastric bleed. [ABSTRACT FROM AUTHOR]

Background: It is not known which risk stratification system has the best discrimination ability for predicting prostate cancer death. Methods: We identified patients with non-metastatic primary prostate adenocarcinoma diagnosis between 2004 and 2015 using the Surveillance, Epidemiology, and End Results database. Patients were categorized in different risk groups using the three frequently used risk stratification systems of the National Comprehensive Cancer Network guideline (NCCN-g), American Urological Association guideline (AUA-g), and European Association of Urology guideline (EAU-g), respectively. Associations between risk classification and prostate cancer-specific mortality (PCSM) were determined using Kaplan–Meier analyses and multivariable regression with Cox proportional hazards model. Area under the receiver operating characteristics curve (AUC) analyses were used to test the discrimination ability of the three risk grouping systems. Results: We analyzed 310,062 patients with a median follow-up of 61 months. A total of 36,368 deaths occurred, including 6,033 prostate cancer deaths. For all the three risk stratification systems, the risk groups were significantly associated with PCSM. The AUC of the model relying on NCCN-g, AUA-g, and EAU-g risk stratification systems for PCSM at specifically 8 years were 0.818, 0.793, and 0.689 in the entire population; 0.819, 0.795, and 0.691 in Whites; 0.802, 0.777, and 0.681 in Blacks; 0.862, 0.818, and 0.714 in Asians; 0.845, 0.806, and 0.728 in Chinese patients. Regardless of the age, marital status, socioeconomic status, and treatment modality, AUC of the model relying on NCCN-g and AUA-g for PCSM was greater than that relying on EAU-g; AUC of the model relying on NCCN-g system was greater than that of the AUA-g system. Conclusions: The NCCN-g and AUA-g risk stratification systems perform better in discriminating PCSM compared to the EAU-g system. The discrimination ability of the NCCN-g system was better than that of the AUA-g system. It is recommended to use NCCN-g to evaluate risk groups for prostate cancer patients and then provide more appropriate corresponding treatment recommendations. [ABSTRACT FROM AUTHOR]

Highlights • Combined toxic effects of UV-B radiation and DEHP on S. acuminatus were investigated. • UV-B radiation decreases photosynthesis and destroys antioxidant system of S. acuminatus. • The addition of low DEHP concentration alleviates the cell damage of S. acuminatus induced by UV-B radiation. • UV-B radiation can photodegrade DEHP via ROS generation in S. acuminatus. Abstract The co-contamination discharge of Phthalate esters (PAEs) by human activities and the increased UV radiation is increasing in aquatic ecosystems. However, little information is available about the combined detrimental effects of UV and PAEs on phytoplankton. In this study, the combined effects of UV-B irradiation and di-(2-ethylhexyl) phthalate (DEHP) on photosynthesis and antioxidant system of Scenedesmus acuminatus , and the DEHP degradation were investigated. Results showed that UV-B radiation decreased the chlorophyll a fluorescence yield, photosynthetic activity (Fv/Fm), pigment content and superoxide dismutase activity. This radiation also increased the reactive oxygen species (ROS) production and soluble protein and malondialdehyde contents. UV-B radiation with 10 mg L−1 DEHP improved the Fv/Fm and alleviated the cell damage of S. acuminatus, and the addition of high DEHP concentration (≥50 mg L−1) aggravated cell damage. The ROS generation also decreased with the increased DEHP concentration. UV-B radiation can effectively promote the DEHP degradation, with the highest degradation rate of 89.9% at an initial DEHP concentration of 10 mg L−1 within 6 h. This result may be attributed to that UV-B irradiance induced DEHP degradation under the regulation of ROS generated by S. acuminatus. Our findings will contribute to the understanding of the combined toxic mechanisms of UV-B and DEHP and in the evaluation of ecological environment risks for primary producers in aquatic ecosystems. [ABSTRACT FROM AUTHOR]

Purpose: In our previous study, we found that AKR1C3 was a radioresistance gene in KY170R cells. Downregulating the expression of AKR1C3 could enhance the radiosensitivity of esophageal carcinoma cells. In this study, we investigated whether methyl jasmonate (MeJ), an inhibitor of Aldo-keto reductase family1 member C3 (AKR1C3), could overcome radiation resistance in AKR1C3 highly expressed cells.Patients and methods: We used clone formation assays to detect radiosensitivity effects. Flow cytometry assays were used to detect reactive oxygen species (ROS) accumulation and apoptosis. Enzyme linked immunosorbent assays (ELISAs) were used to detect the concentrations of prostaglandin F2 (PGF2) and prostaglandin D2 (PGD2) in the cells after incubation with MeJ. Western blotting was used to detect AKR1C3 and peroxisome proliferator-activated receptor gamma (PPARγ) expression.Results: We found that AKR1C3 was highly expressed in radioresistant esophageal carcinoma cells. MeJ inhibited the expression of AKR1C3 and enhanced the radiation sensitivity of esophageal carcinoma cells expressing high levels of AKR1C3 (P [ABSTRACT FROM AUTHOR]

Purpose: Bulky non-small cell lung cancer (NSCLC) is difficult to achieve effective local control by conventionally fractionated radiotherapy (CRT). The present work aims to evaluate the safety and efficacy of partial stereotactic ablative boost radiotherapy (P-SABR) in bulky NSCLC. Patients and methods: From December 2012 through August 2017, 30 patients with bulky NSCLC treated with P-SABR technique were analyzed. The P-SABR plan consisted of one partial SABR plan (5–9 Gy/f, 3–6 fractions) to gross tumor boost (GTVb), followed by one CRT plan to the planning target volume (PTV). GTVb was the max volume receiving SABR to guarantee the dose of organs-at-risks (OARs) falloff to about 3 Gy/f. The total dose of PTV margin was planned to above 60 Gy. The simply CRT plans were created using the same planning parameters as the original plan, with the goal to achieve comparable OARs doses and PTV margin dose to the P-SABR plan. Dosimetric variables were acquired in both P-SABR and compared CRT plans. Toxicity, local control, and survival were also evaluated. Results: Median follow-up in survivors was 10.3 months (range=2.3–39.4 months). Eleven patients (36.7%) had partial response (PR) and ten patients (33.3%) had stable disease (SD). Two-year overall survival was 55.6%. Two-year local control rate was 85.7%. No severe acute side effects.CTCAE Grade III were observed. Compared to the simply CRT plan, P-SABR plans achieved similar doses to the OARs and Dmin, but increased dose at the isocenter, Dmean, Dmax, and biological equivalent dose (BED) significantly (P<0.05). BED in the tumor center could reach 107.3 Gy (93.2–132 Gy). Patients with B90≥65% achieved a higher local control rate than those with B90<65% (P=0.010). Conclusion: This retrospective study suggests that P-SABR is feasible and well tolerated in bulky NSCLC. Local control rate is encouraging, especially for the B90≥65% group, which may due to the ability of P-SABR to optimize BED with equivalent toxicity. [ABSTRACT FROM AUTHOR]

Abstract: In this study, we investigated the combined effects of UV-B irradiation and herbicides (glyphosate, GPS; 2-Methyl-4-chlorophenoxyacetic acid, MCPA-Na; 3-(3,4-dichlorophenyl)-1,1-dimethylurea, DCMU) and the antioxidant (ascorbic acid, ASC) on photosynthesis, antioxidant enzymes and DNA damage in two bloom-forming cyanobacteria, Anabaena sp. and Microcystis viridis. UV-B irradiance increased reactive oxygen species (ROS) production, which decreased chlorophyll a fluorescence yield, pigment content and superoxide dismutase (SOD) activity, and increased malondialdehyde (MDA) content and caused serious DNA damage. The degree of these damages was aggravated by the addition of DCMU, GPS and MCPA, and was partially mitigated by the addition of ASC. During the recovery process, the degree and mechanism in restoring DNA damage and photosynthesis inhibition were different by the removal of UV-B and herbicides (DCMU, GPS and MCPA) in both cyanobacteria. These results suggest that the combination of UV-B and exogenous herbicides have detrimental effects on cyanobacterial metabolism through either a ROS-mediated process or by affecting the electron transport chain, and may cause the shifts in the phytoplankton community. [Copyright &y& Elsevier]

Abstract, Results section, "Two-year overall survival was 55.6%. Two-year local control rate was  85.7%" should read "One-year overall survival was  64.9%. One-year local control rate was 100%".On page 2574, Response and survival outcomes section, 3rd and 4th sentences, "One-year over-all survival was 88.2%. Two-year overall survival was 55.6% (Figure 2A)." should read "One-year over-all survival was 64.9%. Two-year overall survival was 44.5% (Figure 2A)."On page 2574, Response and survival outcomes section, 10th sentence, "Two-year local control rate was 85.7%. (Figure  2B)." should read "Two-year local control rate was 57.1%. (Figure 2B)."On page 2575, Figure 2 legend, "(A) Kaplan–Meier plots of overall survival for all patients. One-year overall survival was  88.2%. Two-year overall survival was 55.6%. (B) Kaplan–Meier plots of local control for all patients. One-year local control rate was 100%. Two-year local control rate was 85.7%. (C) Patients with B90≥ 65% (n=19) achieved a higher local control rate than those with B90< 65% (n=11) (median survival=15.2 months vs 3.5 months, CI=6.8– 23.6 and 2.2– 4.9 months, respectively; P=0.010). (D) Patients with B80≥ 90% (n=20) achieved a higher local control rate than those with B80< 90% (n=10) (median survival=14.9 months vs 3.5 months, CI=3.4– 26.3 and 1.8– 5.2 months, respectively; P=0.045)." should read "(A) Kaplan–Meier plots of overallsurvival for all patients. One-year overall survival was 64.9%. Two-year overall survival was 44.5%. (B) Kaplan–Meier plots of local control for all patients. One-year local control rate was  100%. Two-year local control rate was 57.1%. (C) Patients with B90≥ 65% (n=19) achieved a higher local control rate than those with B90< 65% (n=11) (median survival=15.2 months vs 3.5 months, CI=6.8– 23.6 and 2.2– 4.9 months, respectively; P=0.010). (D) Patients with B80≥ 90% (n=20) achieved a higher local control rate than those with B80< 90% (n=10) (median survival=14.9 months vs 3.5 months, CI=3.4– 26.3 and 1.8– 5.2 months, respectively; P=0.045)."On page 2576, Discussion section, last sentence "Therefore, daily SABR was applied in our article and the 2-year local control rate was as high as 85.7%, even stage IV NSCLC were 40%." should read "Therefore, daily SABR was applied in our article and the 1-year local control rate was as high as 100%, even stage IV NSCLC were 40%."Despite the correction in the text list as above, the Figures of Kaplan–Meier plots of overall survival and local control are correct, and the error doesn't the change the overall findings reported in the paper. We can still conclude that "This retrospective study suggests that P-SABR is feasible and well tolerated in bulky NSCLC. Local control rate is encouraging, especially for the B90≥ 65% group, which may due to the ability of P-SABR to optimize BED with equivalent toxicity". The authors apologize for this error. Read the original article [ABSTRACT FROM AUTHOR]